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1
VRIESENDORP, HUIBERT M., and JERRY WILLIAMS. "RADIATION SENSITIVITY OF TRANSPLANTED BONE MARROW CELLS." Transplantation 46, no. 5 (November 1988): 784. http://dx.doi.org/10.1097/00007890-198811000-00035.
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Reyes, Morayma, Sheng Li, Jessica Foraker, En Kimura, and Jeffrey S. Chamberlain. "Donor origin of multipotent adult progenitor cells in radiation chimeras." Blood 106, no. 10 (November 15, 2005): 3646–49. http://dx.doi.org/10.1182/blood-2004-12-4603.
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AbstractMultipotent adult progenitor cells (MAPCs) are bone marrow-derived stem cells that have extensive in vitro expansion capacity and can differentiate in vivo and in vitro into tissue cells of all 3 germinal layers: ectoderm, mesoderm, and endoderm. The origin of MAPCs within bone marrow is unknown. MAPCs are believed to be derived from the bone marrow stroma compartment as they are isolated within the adherent cell component. Numerous studies of bone marrow chimeras in the human and the mouse point to a host origin of bone marrow stromal cells. Mesenchymal stem cells (MSCs), which coexist with stromal cells, have also been proven to be of host origin after allogeneic bone marrow transplantation in numerous studies. We report here that following syngeneic bone marrow transplants into lethally irradiated C57BL6 mice, MAPCs are of donor origin.
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Greenberger, Joel S., and Michael Epperly. "Bone Marrow–Derived Stem Cells and Radiation Response." Seminars in Radiation Oncology 19, no. 2 (April 2009): 133–39. http://dx.doi.org/10.1016/j.semradonc.2008.11.006.
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Kawata, Yumiko, Eiji Ikami, Junya Nojima, Shoichiro Kokabu, Tetsuya Yoda, and Tsuyoshi Sato. "Effect of Adipose Tissue-Derived Mesenchymal Stem Cells on Irradiated Bone Marrow-Derived Mesenchymal Stem Cells." Journal of Bone Biology and Osteoporosis 4, no. 1 (November 15, 2018): 94–98. http://dx.doi.org/10.18314/jbo.v4i1.1230.
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Adipose-derived Mesenchymal stem cells have emerged as an attractive alternative source of cell therapy. While radiation therapy is an important application for head and neck cancer, the effect of adipose-derived mesenchymal stem cells on irradiated bone marrow-derived Mesenchymal stem cells is still unclear. Herein, we explored how clinical total radiation dose affect gene expression related with differentiation on murine bone marrow-derived mesenchymal stem cells and how murine adipose-derived mesenchymal stem cells affect irradiated murine bone marrow-derived mesenchymal stem cells. The clinical total radiation dose upregulates osterix mRNA expression. Moreover, adiposederived mesenchymal stem cells dramatically promoted the upregulation of osterix mRNA expression whereas inhibited NFATc1 mRNA expression. Taken as a whole, irradiated bone marrow-derived mesenchymal stem cells co-cultured with adipose-derived mesenchymal stem cells may exhibit osteogenic property.
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Mastrogiacomo, M., V. S. Komlev, M. Hausard, F. Peyrin, F. Turquier, S. Casari, A. Cedola, F. Rustichelli, and R. Cancedda. "Synchrotron Radiation Microtomography of Bone Engineered from Bone Marrow Stromal Cells." Tissue Engineering 10, no. 11-12 (November 2004): 1767–74. http://dx.doi.org/10.1089/ten.2004.10.1767.
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Zhang, Zengli, Hongtao Zhang, Fenju Liu, Mingcai Qiu, and Jian Tong. "Effects of Gamma Radiation on Bone-Marrow Stromal Cells." Journal of Toxicology and Environmental Health, Part A 73, no. 7 (February 26, 2010): 514–19. http://dx.doi.org/10.1080/15287390903523477.
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Wang, Ying, Jian-Ming Li, Wayne A. C. Harris, Cynthia R. Giver, and Edmund K. Waller. "Lack of Host Bone Marrow-Derived Interleukin-12 Increased the Incidence of Allograft Rejection in Allogeneic Bone Marrow Transplantation." Blood 118, no. 21 (November 18, 2011): 2960. http://dx.doi.org/10.1182/blood.v118.21.2960.2960.
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Abstract Abstract 2960 Background: Donor cell engraftment following allogeneic bone marrow transplantation (BMT) is affected by several factors, including immunological major histocompatibility complex (MHC) barriers, the intensity of the conditioning regimen, and the content of T-cells in the graft. The current model for engraftment in allogeneic BMT is that host dendritic cells (DCs) activate donor T-cells which promote engraftment by eliminating radio-resistant cytotoxic host immune cells, especially natural killer (NK) cells and T-cells. To explore the interaction between donor T-cell and host antigen-presenting cells (APC) in engraftment in allogeneic BMT, we focused on the role of interleukin-12 (IL-12), a key cytokine produced mainly by DCs that drives the development of donor type 1 helper T cells (Th1) and type 1 cytotoxic T lymphocytes (Tc1). Methods: Radiation chimeras with >95% donor chimerism were created by transplanting 5 × 106 bone marrow (BM) cells from IL-12 knock out (IL-12 KO) or wild type (WT) B6 (H-2Kb, CD45.2) donors into congenic BL6 Pepboy (B6.SJL-PtprcaPep3b/BoyJ, H-2Kb, CD45.1) mice following lethal 11 Gy irradiation. A second allogeneic BMT was conducted 2 months later using MHC mismatched FVB (H-2q, CD45.1), BA.B10 (H-2Kk, CD45.2, CD90.1) or B10.BR (H-2Kk, CD45.2, CD90.2) donor cells. In vivo bioluminescent imaging (BLI) was performed to analyze the number and in vivo distribution of luciferase+ donor T-cells. The whole-body bioluminescent signal was used as a marker of the donor T cell expansion. Engraftment of donor myeloid cells was determined by flow cytometry using mAbs for specific leukocyte markers expressed on donors and recipients (CD45.1, CD45.2, H-2Kb). Intracellular cytokine expression (IL-4, IL-10, IFN-g) by donor CD4+ and CD8+ T cells was analyzed by flow cytometry. Results: WT BL6→BL6 radiation chimeras recipients showed greater expansion of luciferase+ donor T-cells compared with IL-12 KO BL6→BL6 radiation chimeras recipients and FVB→FVB syngeneic recipients at early time point (2 wks) following 9 Gy re-irradiation and transplantation of 3 × 105 luciferase+ FVB-L2G85 T-cells in combination with 5 × 106 T cell depleted (TCD) BM cells from FVB mice following (Fig 1). At 4 weeks post transplant, more WT BL6→BL6 radiation chimeras achieved myeloid engraftment than IL-12 KO BL6→BL6 radiation chimera recipients(75.0% versus 33.3% respectively, p = 0.086), and the former group had better erythroid engraftment than the latter group (RBC 8.65 ± 1.88 × 1012/L versus 5.67 ± 2.22 × 1012/L respectively, p = 0.011). However, when FVB, WT BL6→BL6 or IL-12 KO BL6→BL6 radiation chimeras recipients were conditioned with a larger dose of irradiation prior to the second transplantation (10 Gy) and received a larger dose of donor T-cells (5 × 105), both the WT BL6→BL6 and IL-12 KO BL6→BL6 radiation chimeras recipients achieved full donor engraftments (85.7% versus 87.5% respectively, p = NS). Donor T cells in allogeneic BMT recipients were Th1/Tc1 polarized, there were no differences in frequencies and total numbers of Th1/Tc1 donor CD4+ and CD8+ T cells comparing recipients of WT BL6→BL6 and IL-12 KO BL6→BL6 radiation chimeras. In spite of an increased irradiation dose and larger number of donor T-cells in the second transplant regimen, no increase in graft versus host disease (GVHD) clinical scores and GVHD-mortality were observed in the recipients of WT BL6→BL6 radiation chimeras compared with recipients of IL-12 KO BL6→BL6 radiation chimeras. Conclusion: These data support a role for host BM-derived IL-12 in facilitating engraftment in allogeneic BMT following a reduced dose (9 Gy) radiation. The lack of host BM-derived IL-12 expression led to allograft rejection. Rejection could be overcome by increasing the dose of pre-transplant irradiation and the content of donor T-cells without causing lethal GVHD. As the main source of host BM-derived IL-12, recipient APC thus play an important role in donor T-cell activation. As has been previously demonstrated in a murine BMT model, the addition of IL-12 in the peri-transplant period helped to separate graft versus leukemia effects from the GVHD-promoting activity of donor T-cells (Yang, 1997). Patients predicted to be high risk of graft failure may benefit from treatment strategies that contribute to production of IL-12 during the early phases of hematopoietic engraftment. Disclosures: No relevant conflicts of interest to declare.
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Bilko, N. M., I. S. Dyagil, I. S. Russu, and D. I. Bilko. "CIRCULATING HEMATOPOIETIC PROGENITOR CELLS IN PATIENTS AFFECTED BY CHORNOBYL ACCIDENT." Experimental Oncology 38, no. 4 (December 22, 2016): 242–44. http://dx.doi.org/10.31768/2312-8852.2016.38(4):242-244.
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High radiation sensitivity of stem cells and their ability to accumulate sublethal radiation damage provides the basis for investigation of hematopoietic progenitors using in vivo culture methodology. Unique samples of peripheral blood and bone marrow were derived from the patients affected by Chornobyl accident during liquidation campaign. Aim: To investigate functional activity of circulating hematopoietic progenitor cells from peripheral blood and bone marrow of cleanup workers in early and remote periods after the accident at Chornobyl nuclear power plant (CNPP). Materials and Methods: The assessment of the functional activity of circulating hematopoietic progenitor cells was performed in samples of peripheral blood and bone marrow of 46 cleanup workers, who were treated in the National Scientific Center for Radiation Medicine of the Academy of Medical Sciences of Ukraine alongside with 35 non radiated patients, who served as a control. Work was performed by culturing peripheral blood and bone marrow mononuclear cells in the original gel diffusion capsules, implanted into the peritoneal cavity of CBA mice. Results: It was shown that hematopoietic progenitor cells could be identified in the peripheral blood of liquidators of CNPP accident. At the same time the number of functionally active progenitor cells of the bone marrow was significantly decreased and during the next 10 years after the accident, counts of circulating progenitor cells in the peripheral blood as well as functionally active hematopoietic cells in bone marrow returned to normal levels. Conclusion: It was shown that hematopoietic progenitor cells are detected not only in the bone marrow but also in the peripheral blood of liquidators as a consequence of radiation exposure associated with CNPP accident. This article is a part of a Special Issue entitled “The Chornobyl Nuclear Accident: Thirty Years After”.
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De Lisio, Michael, Nghi Phan, Douglas R. Boreham, and Gianni Parise. "Exercise-induced protection of bone marrow cells following exposure to radiation." Applied Physiology, Nutrition, and Metabolism 36, no. 1 (January 2011): 80–87. http://dx.doi.org/10.1139/h10-087.
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The hormetic effects of exercise training have previously been shown to enhance cellular protection against oxidative stress. Therefore, adaptations to exercise training may attenuate the harmful effects of radiation induced by oxidative stress. Flow cytometric analysis of genotoxicity (γH2AX foci and micronucleated reticulocytes (MN-RET)) and cytotoxicity (apoptosis and percentage of reticulocytes) were conducted on bone marrow cells isolated from acutely exercised (Acute EX), exercise-trained (EX), and sedentary (SED) mice following 1 and 2 Gy radiation challenges in vitro. Acute EX increased the percentage of cells with activated caspase-3 and -7 (32%, p < 0.001) and γH2AX foci formation in response to 2 Gy radiation challenge (10%, p < 0.05). Exercise training significantly attenuated γH2AX foci formation and MN-RET production in response to 1 Gy radiation challenge (18%, p < 0.05 and 22%, p < 0.05, respectively). Exercise training also significantly reduced basal percentages of cells with activated caspase-3 and -7 and in response to radiation in bone marrow cells (11%, p < 0.05). These results suggest that oxidative stress caused by acute exercise induces an adaptive response responsible for the radioprotective effects of exercise training.
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Ferrant, A., M. Cogneau, N. Leners, F. Jamar, P. Martiat, and JL Michaux. "52Fe for additional marrow ablation before bone marrow transplantation." Blood 81, no. 12 (June 15, 1993): 3435–39. http://dx.doi.org/10.1182/blood.v81.12.3435.3435.
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Abstract The effectiveness of bone marrow transplantation (BMT) for malignant blood diseases remains limited by the inability of the preparative regimen to eliminate the disease without causing toxicity to normal organs. We have used 52Fe to deliver radiotherapy selectively to the BM. Fourteen patients with hematologic malignancies received 52Fe before a conventional BMT conditioning regimen. The median 52Fe dose was 58 mCi (range, 32 to 85 mCi). As evaluated by quantitative scanning, the median percentage of 52Fe taken up by the BM was 82% (range, 36% to 90%). This resulted in a median radiation-absorbed dose to the BM of 632 rad (range, 151 to 1,144 rad). The median uptake of 52Fe by the liver was 18% (range, 10% to 64%) and the median radiation-absorbed dose to the liver was 239 rad (range, 82 to 526 rad). The median whole body radiation-absorbed dose was 46 rad (range, 22 to 68 rad). No untoward effects were noted after the injections of 52Fe. The patients recovered hematopoiesis without toxicity in excess of that expected with conventional conditioning alone. The median follow-up was 8 months and three patients have relapsed. 52Fe should provide a way to boost the radiation dose to marrow-based diseases before marrow transplantation without increasing toxicity.
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Ferrant, A., M. Cogneau, N. Leners, F. Jamar, P. Martiat, and JL Michaux. "52Fe for additional marrow ablation before bone marrow transplantation." Blood 81, no. 12 (June 15, 1993): 3435–39. http://dx.doi.org/10.1182/blood.v81.12.3435.bloodjournal81123435.
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The effectiveness of bone marrow transplantation (BMT) for malignant blood diseases remains limited by the inability of the preparative regimen to eliminate the disease without causing toxicity to normal organs. We have used 52Fe to deliver radiotherapy selectively to the BM. Fourteen patients with hematologic malignancies received 52Fe before a conventional BMT conditioning regimen. The median 52Fe dose was 58 mCi (range, 32 to 85 mCi). As evaluated by quantitative scanning, the median percentage of 52Fe taken up by the BM was 82% (range, 36% to 90%). This resulted in a median radiation-absorbed dose to the BM of 632 rad (range, 151 to 1,144 rad). The median uptake of 52Fe by the liver was 18% (range, 10% to 64%) and the median radiation-absorbed dose to the liver was 239 rad (range, 82 to 526 rad). The median whole body radiation-absorbed dose was 46 rad (range, 22 to 68 rad). No untoward effects were noted after the injections of 52Fe. The patients recovered hematopoiesis without toxicity in excess of that expected with conventional conditioning alone. The median follow-up was 8 months and three patients have relapsed. 52Fe should provide a way to boost the radiation dose to marrow-based diseases before marrow transplantation without increasing toxicity.
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Porter, Rebecca L., and Laura M. Calvi. "Prostaglandin E2 Is Rapidly Produced In Response to Bone Marrow Injury and Improves Survival of Primitive Hematopoietic Cells." Blood 116, no. 21 (November 19, 2010): 407. http://dx.doi.org/10.1182/blood.v116.21.407.407.
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Abstract Abstract 407 Since the hematopoietic system is exquisitely sensitive to environmental and iatrogenic injury, the bone marrow microenvironment likely provides protective mechanisms during times of injury or stress. We have previously demonstrated that prostaglandin E2 (PGE2), which can be produced by many cell types in the bone marrow, targets both the bone marrow microarchitecture and primitive hematopoietic cells when administered systemically to mice (Porter, Frisch et. al., Blood, 2009). Since PGE2 is a local mediator of injury and is known to play a protective role in other cell types, we hypothesized that it could be an important microenvironmental regulator of HSPCs during times of injury. To test this hypothesis, we injured mice with a sub-lethal dose of gamma radiation, 6.5 Gy TBI, and sacrificed mice at varying time points from 1 hour to 6 days post-radiation. Bone marrow supernatant was collected and used for quantification of local PGE2 levels by ELISA. We found that, compared to non-irradiated mice, the PGE2 levels were increased greater than two-fold by 4 hours after irradiation (p=0.0030; n=3–6 mice/group), and these levels remain elevated until at least 6 days after injury (p<0.0001 by ANOVA). These data clearly demonstrate that PGE2 production is rapidly upregulated following bone marrow injury. To determine if HSPCs could be responding to this increase in local PGE2, we sorted Lin− c-Kit+ Sca1+ (LSK) cells from murine bone marrow and assayed the expression of the four PGE2 receptors, EP1-EP4. RT-PCR analysis demonstrated that all four receptors are expressed on LSK cells, suggesting that PGE2 could be acting on these primitive hematopoietic cells during times of injury. We next tested whether supplying additional PGE2 to mice could protect hematopoietic cells after injury. Mice were subjected to 6.5 Gy TBI and were treated with 0.5 mg/kg 16,16-dimethyl-PGE2 (dmPGE2) immediately after radiation and once daily thereafter until time of sacrifice. At 24 hours after radiation injury, mice that were treated with dmPGE2 had greater than 8-fold more surviving LSK cells, a population which still retains HSC repopulating activity in competitive transplantation studies, in their bone marrow compared with vehicle treated mice (n=4/group, p=0.046). Similarly, at 72 hr post-radiation, the dmPGE2 treated mice continued to have almost 2-fold greater numbers of LSK cells remaining viable in their bone marrow compared with vehicle treated mice (n=2–3/group). These data suggest that dmPGE2 treatment after bone marrow injury may provide protection, at least in the days immediately following injury, to primitive hematopoietic cells that remain capable of regenerating the hematopoietic system. To further support this idea, we also pretreated uninjured bone marrow cells in vitro with PGE2 (1 μ M) for 90 minutes and then exposed them to the chemotherapeutic agent cytarabine (Ara-C, 10 μ M for 4 hours). Pretreatment with PGE2 results in lower levels of apoptotic LSK cells compared with vehicle pre-treated LSK cells (30.26% vs. 39.02%; n=9/group; 3 independent experiments; p=0.0012). This result correlates with our in vivo radiation injury data and suggests that PGE2 may target primitive hematopoietic cells and render them more resistant to cell death from injury. Taken together, these results suggest that PGE2, which is released in the bone marrow after radiation exposure, may be an important microenvironmental regulator of HSPC response to injury, by preventing cell death, and/or increasing their recovery. Amplification of this physiological signal by treatment with exogenous PGE2 could provide a beneficial means of protecting hematopoietic cells in clinical situations of hematopoietic system injury and bone marrow transplantation, allowing patients to tolerate bone marrow suppressive treatments or to recover more easily. Further, these results also bring forth a potential concern about the safety of blocking prostaglandin synthesis by using anti-inflammatory medications during times of bone marrow injury. Disclosures: No relevant conflicts of interest to declare.
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Wang, D. W., R. Y. Peng, and C. Q. Xiong. "Molecular Pathologic Studies on the Echanisms of Radiation-Induced Hematopoietic Cells Apoptosis and the Recovery in Mouse Bone Marrow." Microscopy and Microanalysis 4, S2 (July 1998): 1078–79. http://dx.doi.org/10.1017/s1431927600025514.
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There have rarely been reported on radiation induced hematopoietic cells apoptosis and the recovery ,the expression and significance of oncogenes, tumor suppresser genes, hematopoietic grouth factors and their receptors in bone marrow.By meams of routine pathology, specific stainning, electron microscope, immunocytochemistry, image analysis, in situ hybridization, in situ terminal end labelling, in situ PCR and DNA electrophoresis, The machanisms of hematopoietic cells apoptosis and then recovery in mouse bone marrow were studies through LAC A mouse total body irradiation with 60Co γ -rays.The results showed: The bone marrow in each radiated group appeared obvious injury and then recovery, and the lessions were the most typical in 5.5Gy irradiation group, the pathologic changes were divided into four phases: namely the phase of hematopoietic cells apoptosis,bone marrow at 6hours after radiation. Furthermore, the higher radiation dose, the more the apoptotic cells were(table l).
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Butturini, A., RC Seeger, and RP Gale. "Recipient immune-competent T lymphocytes can survive intensive conditioning for bone marrow transplantation." Blood 68, no. 4 (October 1, 1986): 954–56. http://dx.doi.org/10.1182/blood.v68.4.954.954.
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Abstract Bone marrow transplantation is usually preceded by intensive chemotherapy and radiation therapy designed to completely eliminate recipient immune-competent cells that might reject the donor bone marrow. We show that seven of 14 bone marrow transplant recipients who received intensive conditioning retained circulating T lymphocytes that proliferate after incubation with interleukin 2 and phytohemagglutinin and function as effector cells in an in vitro model of graft rejection. These T cells may mediate graft rejection.
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Butturini, A., RC Seeger, and RP Gale. "Recipient immune-competent T lymphocytes can survive intensive conditioning for bone marrow transplantation." Blood 68, no. 4 (October 1, 1986): 954–56. http://dx.doi.org/10.1182/blood.v68.4.954.bloodjournal684954.
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Bone marrow transplantation is usually preceded by intensive chemotherapy and radiation therapy designed to completely eliminate recipient immune-competent cells that might reject the donor bone marrow. We show that seven of 14 bone marrow transplant recipients who received intensive conditioning retained circulating T lymphocytes that proliferate after incubation with interleukin 2 and phytohemagglutinin and function as effector cells in an in vitro model of graft rejection. These T cells may mediate graft rejection.
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Khan, Azhar M., Tahleel A. Shera, Naseer A. Choh, Gh Mohammad Wani, and Zubair Ahmad. "Radiation Protection in Pediatric Radiology." JMS SKIMS 19, no. 1 (June 16, 2016): 39–40. http://dx.doi.org/10.33883/jms.v19i1.285.
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The radiation risk is higher for children than for adults, as children's tissues have a higher cell division rate, and cells can be damaged during this process. Children's bodies also have a higher water content and therefore absorb more radiation, which can cause damage to their genes. There are radiation, which can cause damage to their genes. There are also differences in the location of particularly at-risk tissues such as hematopoietic bone marrow. In adults, 74% (spine ribs, pelvis) is located in the skeleton or the trunk, and only 9% in the extremities. In infants, 29% is located in the skeleton of the trunk and 35% in the extremities.In adults, 8% is located in the cranial bones; in infants, 27%. This means that infants have large proportions of hematopoietic bone marrow in all parts of the body, including the extremities and any radiograph irradiates a substantial proportion of the hematopoietic marrow. As radiation induced malignant lesions remain latent for years, children and adolescents are prone to experience them. JMS 2016; 19(1):39-40
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Liu, Hua-qing, Bing-Yan Li, Zeng-Li Zhang, and Jian Tong. "Ionizing radiation stimulates osteoclast development in mice bone marrow cells and RAW264.7 cells." Bone 47 (October 2010): S417—S418. http://dx.doi.org/10.1016/j.bone.2010.09.227.
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Qomariyah, Nurul, Muhaimin Rifa’i, and Unggul P. Juswono. "Effects of Gamma Radiation Exposure to Hematopoietic Cells on Bone Marrow." Natural B 3, no. 1 (April 1, 2013): 19–25. http://dx.doi.org/10.21776/ub.natural-b.2013.002.01.4.
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Storb, Rainer. "Bone Marrow Transplantation for Aplastic Anemia." Cell Transplantation 2, no. 5 (September 1993): 365–79. http://dx.doi.org/10.1177/096368979300200503.
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The increased survival of aplastic anemia patients treated by human leukocyte antigens (HLA)-identical marrow transplants is due in part to a decrease in the incidence of graft rejection. The decrease in rejection, in turn, results from the more judicious use of transfusions before transplant, the removal of sensitizing white blood cells from transfusion products, and improvements in the immunosuppressive conditioning programs used to prepare patients for transplant. In regards to the latter, radiation-based programs have been effective, although a cydophosphamide/antithymocyte globulin program begins to look impressive with only one rejection among 33 patients transplanted. In regards to transfusions before transplant, in vitro radiation of all blood products may further reduce the risk of sensitization to minor histocompatibility antigens in the future. The incidence and severity of acute graft-versus-host disease (GvHD) have declined with the use of the methotrexate/cyclosporine regimen, and this has also contributed to improved survival. Chronic GvHD is difficult to treat and future emphasis should be on prevention rather than on treatment. Whether an extended course of cyclosporine beyond 6 mo after transplant will reduce the risk of chronic GvHD is under study. As more and more patients become long-term survivors, problems from long-term sequelae from the conditioning programs and from postgrafting immunosuppression must be considered, in particular secondary malignancies. Perhaps less toxic conditioning programs can be designed. Because of the higher likelihood of causing secondary cancer, possible deleterious effects on growth and development for pediatric patients, and the problem of sterility, radiation-based regimens should not be used in HLA-identical recipients.
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Epperly, Michael W., Darcy Franicola, Tracy Dixon, Xichen Zhang, Paavani Komanduri, Benjamin Greenberger, Peter Wipf, Kazunori Koide, and Joel S. Greenberger. "Bone Marrow Small Molecule Radioprotectors." Blood 110, no. 11 (November 16, 2007): 4096. http://dx.doi.org/10.1182/blood.v110.11.4096.4096.
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Abstract Development of small molecule radioprotectors is a major national priority. Two groups of compounds have particular promise. The first group targets the mitochondria based upon previous data with transgene MnSOD which when expressed in the mitochondria prevents apoptosis and increases radioprotection. These agents contain the antioxidant tempol or nitric oxide synthetase inhibitor 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT) attached to a hemi-gramicidin linker which targets the mitochondria. The second group consists of the dietary agent resveratrol and acetylated variants. Mouse hematopoietic progenitor 32Dcl3 cells were incubated for 1 hr in 10 μM tempol, AMT, or gramicidin linked tempol XJB-5-125 (tempol), XJB-7-75 (tempol) or JP4-039 (AMT). In separate experiments, 32Dcl3 cells were incubated for 1 hr in resveratrol or acetylated resveratrol. The cells were then irradiated to doses ranging from 0 to 8 Gy, plated in 0.8% methylcellulose, and incubated in a 5% CO2 incubator for 7 days. Colonies of greater than 50 cells were counted with the data analyzed using linear quadratic or single-hit, multi-target models. 32Dcl3 cells incubated in 10 μm tempol before irradiation resulted in no change in radiation sensitivity while incubation in XJB-5-125 or XJB-7-75 had decreased radiosensitivity. XJB-5-125 had an increased Do of 1.91 ± 0.67 Gy compared to 1.32 ± 0.09 Gy for 32Dcl3 cells incubated in tempol and 1.35 ± 0.27 Gy for control 32Dcl3 cells (p = 0.045 or 0.040, respectively). Incubation in XJB-5-75 resulted in an increased shoulder on the survival curve with an ñ of 19.4 ± 2.6 compared to 8.7 + 1.6 for cells incubated in tempol or 6.9 +1.8 for control 32Dcl3 cells (p = 0.025 or 0.022). Incubation in JP4-039 resulted in an increased Do of 2.2 ± 0.1 Gy compared to 1.24 ± 0.15 or 1.13 ± 0.06 for cells incubated in AMT or control 32Dcl3 cells only, respectively (p = 0.0115 or 0.0098, respectively). Incubation of 32Dcl3 cells in resveratrol or acetylated resveratrol before irradiation resulted in an increased shoulder on the survival curve of 33.2 ± 5.7 or 57.5 ± 9.9, respectively, compared to 6.9 ± 1.8 for 32Dcl3 cells (p = 0.0122 or 0.0072, respectively). These compounds were tested in mice receiving an LD50/30 irradiation dose. C57BL/6NHsd mice were injected intraperitoneally with 10 mg/kg of XJB-5-125, XJB-7-75or JP4-039 or 25 mg/kg of resveratrol or acetylated resveratrol and irradiated 10 mins later along with control mice to 9.5 Gy whole body irradiation. The mice injected with XJB-5-125, XJB-7-75, JP4-039 or acetylated-resveratrol had increased survival compared to control irradiated mice (p ≤ 0.0004). Therefore, four new small molecules have been identified which demonstrate significant radioprotective properties both in vitro and in vivo.
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Gupta, Mamta, Shiv K. Gupta, Barbara Hoffman, and Dan A. Liebermann. "Gadd45a and Gadd45b Protect Haematopoetic Cells from Ultraviolet Radiation Induced Apoptosis Via Distinct Signaling Pathways." Blood 104, no. 11 (November 16, 2004): 1258. http://dx.doi.org/10.1182/blood.v104.11.1258.1258.
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Abstract Gadd45 expression, which is stress inducible, has been associated with growth arrest, but the exact role of gadd45 family genes in apoptosis still remains unclear. We have found that myeloid progenitor cells from gadd45a and gadd45b-deficient mice are more sensitive to ultra-violet radiation, VP-16 or daunorubicin induced apoptosis. indicating that gadd45a or gadd45b protect haematopoetic cells from DNA damaging agents. To determine, how gadd45a or gadd45b proteins exert their anti-apoptotic function, bone marrow cells from wild-type and gadd45a or gadd45b deficient mice were exposed to ultraviolet radiation (UV) and analyzed for expression of stress responsive kinases, including JNK and p38. It was observed that P38 and JNK were activated in wt bone marrow cells in response to UV but not in bone marrow cells defecient in gadd45a. Also, the transcription factor NF-kB was activated in wt bone marrow cells, but not in gadd45a−/− cells. The pharmacological inhibitor SB203580 specific for p38, increased apoptosis in reponse to UV, indicating that p38 is implicated in signaling myeloid cell survival. SB203580 was observed also to inhibit the expression of certain NF-kB target genes, including cIAP-1, c-IAP-2, bcl-2 and bcl-xl, in gadd45a+/+ cells but not in gadd45a deficient bone marrow cells. Taken together this data provides first evidence for the role gadd45a plays in the control of hematopoietic cell survival in response to UV, via modulation of P38 MAPK and NF-kB signaling pathways. Unlike in gadd45a−/− bone marrow cells, p38 activation appeared not to be impaired in gadd45b−/− cells, indicating that gadd45b is not involved in p38 activation in myeloid cells. However, UV induced JNK activation was sustained in gadd45b−/− myeloid cells compared to wt cells, indicating that gadd45b is a negative modulator of UV induced JNK signaling in myeloid cells. UV induced activation of MKK4 an upstream regulator of JNK also was impaired in gadd45b−/−. NF-kB was also found activated in wt cells, but not in gadd45b−/− cells. This data indicates that in bone marrow cells exposed to UV, NF-kB induced expression of Gadd45b plays a protective role against UV induced apoptosis via inhibition of MKK4 kinase which in turn results in suppression of JNK activity. Taken together this data provides evidence that Gadd45a and Gadd45b protect haematopoetic cells from genotoxic-stress induced apoptosis via distinct signaling pathways.
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Song, Yimeng, Songling Hu, Junling Zhang, Lin Zhu, Xinrui Zhao, Qianping Chen, Jianghong Zhang, Yang Bai, Yan Pan, and Chunlin Shao. "Fractionated Irradiation of Right Thorax Induces Abscopal Damage on Bone Marrow Cells via TNF-α and SAA." International Journal of Molecular Sciences 22, no. 18 (September 15, 2021): 9964. http://dx.doi.org/10.3390/ijms22189964.
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Radiation-induced abscopal effect (RIAE) outside of radiation field is becoming more attractive. However, the underlying mechanisms are still obscure. This work investigated the deleterious effect of thoracic irradiation (Th-IR) on distant bone marrow and associated signaling factors by irradiating the right thorax of mice with fractionated doses (8 Gy × 3). It was found that this localized Th-IR increased apoptosis of bone marrow cells and micronucleus formation of bone marrow polychromatic erythrocytes after irradiation. Tandem mass tagging (TMT) analysis and ELISA assay showed that the concentrations of TNF-α and serum amyloid A (SAA) in the mice were significantly increased after Th-IR. An immunohistochemistry assay revealed a robust increase in SAA expression in the liver rather than in the lungs after Th-IR. In vitro experiments demonstrated that TNF-α induced SAA expression in mouse hepatoma Hepa1–6 cells, and these two signaling factors induced DNA damage in bone marrow mesenchymal stem cells (BMSCs) by increasing reactive oxygen species (ROS). On the other hand, injection with TNF-α inhibitor before Th-IR reduced the secretion of SAA and attenuated the abscopal damage in bone marrow. ROS scavenger NAC could also mitigated Th-IR/SAA-induced bone marrow damage in mice. Our findings indicated that Th-IR triggered TNF-α release from lung, which further promoted SAA secretion from liver in a manner of cascade reaction. Consequently, these signaling factors resulted in induction of abscopal damage on bone marrow of mice.
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Aliotta, Jason M., Michael Del Tatto, Mark Dooner, Mandy Pereira, and Peter J. Quesenberry. "Bone Marrow Transplant Induces Pulmonary Vascular Remodeling in Mice." Blood 114, no. 22 (November 20, 2009): 4480. http://dx.doi.org/10.1182/blood.v114.22.4480.4480.
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Abstract Abstract 4480 Objective Pulmonary complications are common in bone marrow transplant (BMT) recipients and often of an infectious etiology or attributed to intensive conditioning regimens. Cases of pulmonary arterial hypertension have been described in the setting of autologous BMT but are believed to be the result of acquired infections or previously-administered chemotherapy. Whether transplanted marrow cells themselves are toxic to the recipient's lungs is unknown. Methods To address this, non-irradiated female BALB/C mice were transplanted with 5-6×107 whole bone marrow (WBM) cells from male BALB/C mice daily for four days on week zero, then again on week eight (4.5×108 cells total/mouse), or an equal volume of diluent (control). On week 24, transplanted mice received 1000 cGy of chest-only radiation or no radiation. On week 32, histochemical and immunohistochemical analyses were performed on recipient's lungs. Results Bone marrow chimerism was not significantly different in the irradiated and non-irradiated cohorts at the time of sacrifice (average 45.11+6.25% Y chromosome+, all mice). Recipient lungs contained few non-hematopoietic donor marrow-derived cells. These cells were exclusively epithelial (Y+/cytokeratin+), primarily type II pneumocytes (Y+/prosurfactant C+), while no endothelial (Y+/von Willebrand+) or vascular smooth muscle (Y+/alpha-actin+) cells were identified. Irradiated and non-irradiated cohorts had similar quantities of these cells (0.80+0.22% vs. 0.51+0.08% Y+/cytokeratin+; 0.37+0.08% vs. 0.32+0.12% Y+/prosurfactant C+, p>0.2). Pulmonary vessel wall thickness-to-blood vessel diameter ratios (PVWT/D) were significantly increased in the non-irradiated cohort compared with controls and these ratios were further increased in the irradiated cohort (141+5.75%, 161+5.34% of control, p<0.05 comparing all groups). Conclusions These data indicated that marrow cell infusion alone results in pulmonary vascular remodeling and this effect is augmented by radiation injury. These changes are independent of transplanted marrow cell conversion to pulmonary vascular endothelial, smooth muscle cells. These studies suggest that transplanted cells may be lung toxic entities in the setting clinical BMT. Disclosures: No relevant conflicts of interest to declare.
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Carbonneau, Cynthia L., Geneviève Despars, Shanti Rojas-Sutterlin, Audrey Fortin, Oanh Le, Trang Hoang, and Christian M. Beauséjour. "Ionizing radiation–induced expression of INK4a/ARF in murine bone marrow–derived stromal cell populations interferes with bone marrow homeostasis." Blood 119, no. 3 (January 19, 2012): 717–26. http://dx.doi.org/10.1182/blood-2011-06-361626.
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Abstract Alterations of the BM microenvironment have been shown to occur after chemoradiotherapy, during aging, and after genetic manipulations of telomere length. Nevertheless, whether BM stromal cells adopt senescent features in response to these events is unknown. In the present study, we provide evidence that exposure to ionizing radiation (IR) leads murine stromal BM cells to express senescence markers, namely senescence-associated β-galactosidase and increased p16INK4a/p19ARF expression. Long (8 weeks) after exposure of mice to IR, we observed a reduction in the number of stromal cells derived from BM aspirates, an effect that we found to be absent in irradiated Ink4a/arf-knockout mice and to be mostly independent of the CFU potential of the stroma. Such a reduction in the number of BM stromal cells was specific, because stromal cells isolated from collagenase-treated bones were not reduced after IR. Surprisingly, we found that exposure to IR leads to a cellular nonautonomous and Ink4a/arf-dependent effect on lymphopoiesis. Overall, our results reveal the distinct sensitivity of BM stromal cell populations to IR and suggest that long-term residual damage to the BM microenvironment can influence hematopoiesis in an Ink4a/arf-dependent manner.
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Bing, So Jin, Jinhee Cho, Areum Kim, Kalahe Hewage Iresha Nadeeka Madush Herath, Ginnae Ahn, Nam Ho Lee, Jae Woo Park, and Youngheun Jee. "Geraniin Promotes Recovery of Hematopoietic Cells after Radiation Injury." American Journal of Chinese Medicine 45, no. 05 (January 2017): 1003–16. http://dx.doi.org/10.1142/s0192415x17500537.
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Cells of the hematopoietic system are uniquely radiosensitive due to their rapid proliferation. Consequently, immune suppression readily and undesirably results from irradiation. Our previous studies demonstrated that geraniin isolated from Nymphaea tetragona var. angusta (water lily) had a protective effect on the splenocytes and intestinal tract of irradiated mice. This study was designed to assess the effectiveness of geraniin, an ellagitannin isolated from the water lily, in decreasing gamma ray irradiation-induced destruction of the hematopoietic system in mice. Geraniin treatment improved the survival time of bone marrow cells and maintained bone marrow integrity and also up-regulated the expression of stem cell receptors and the extent of cell mitosis. Geraniin also enhanced the proliferation and differentiation of immune cells that had been suppressed by irradiation. These results suggest geraniin is a promising agent for reconstituting hematopoietic cells after exposure to irradiation.
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Lim, Yiting, Mohammad Hedayati, Akil Merchant, Yonggang Zhang, Theodore DeWeese, and William Matsui. "Improved Survival and Recovery of Hematopoiesis Following Lethal Radiation by Chloroquine-Mediated Activation of ATM." Blood 116, no. 21 (November 19, 2010): 2228. http://dx.doi.org/10.1182/blood.v116.21.2228.2228.
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Abstract Abstract 2228 Irreversible bone marrow damage and impaired blood formation is the primary cause of death following exposure to high doses of radiation. Moreover, the rate at which radiation is delivered may have a profound impact on cytotoxicity; prolonged exposure at a low dose-rate (LDR; 9.4 cGy/hr) has been found to induce greater cell death than the same total dose given at a high dose-rate (HDR; 4500 cGy/hr). Few non-toxic agents are presently available that can offer substantial protection against radiation induced bone marrow failure and death, especially during LDR exposure. We previously demonstrated that chloroquine, a commonly used agent in the treatment of malaria and rheumatologic diseases, can prevent LDR radiation induced cytotoxicity of cell lines in vitro and studied its effects on hematopoiesis in vivo. We initially quantified the effects of LDR radiation on C57/B6 mice and found that 9 Gy delivered at 9.4 cGy/hr for 95.7 hrs induced death in 13/19 (68%) of animals at 15–35 days after radiation. The administration of syngeneic bone marrow cells (1 × 106 cells) immediately after LDR radiation completely rescued animals (10/10) demonstrating that bone marrow failure was responsible for LDR radiation induced death similar to HDR radiation. Next we treated mice with chloroquine (0.0594 mg/17g body weight, i.p.) 24 hrs and 4 hrs prior to exposure to LDR radiation and found that it significantly improved survival (80%, p < 0.05) compared to untreated animals exposed to LDR radiation (32%). We examined hematopoietic recovery following LDR radiation and found that the peripheral WBC was significantly greater in mice treated receiving chloroquine (3.4 × 106/ml vs 1.1 × 106/ml at day 16, p<0.05). Similarly, we found that in vivo chloroquine treatment significantly increased the recovery of bone marrow myeloid CFC (p=0.02), suggesting that it impacted myeloid progenitors. To further validate this finding, we transplanted bone marrow from LDR irradiated mice into lethally irradiated CD45 congenic recipient mice, and found a significant improvement in early engraftment (4.2% vs. 0.4% engraftment at 6 weeks post-transplant, p=0.015). Chloroquine has been found to protect cancer cell lines from LDR radiation in vitro by activating ATM, an essential DNA damage sensor. We examined the effect of chloroquine on ATM and treated unradiated lin- bone marrow cells with chloroquine in vitro (35 ug/ml, 2 hr). Compared to control cells, chloroquine treated cells expressed 2.5-fold more phosphorylated ATM suggesting that the activation of ATM by chloroquine abrogated the lethal effects of LDR radiation in hematopoietic progenitors. We confirmed that ATM was required for chloroquine-mediated radioprotection by studying ATM null mice. In contrast to wild type mice, chloroquine treatment failed to protect ATM null mice from LDR radiation (9 Gy total) with 8/13 (62%) and 9/13 (69%) of animals surviving in treated or non treated mice, respectively (p=0.86). These data suggest that chloroquine exerts a radioprotective effect from LDR radiation by activating ATM in vivo, and may represent a novel means of limiting acute bone marrow failure in the event of widespread environmental LDR radiation exposure. Disclosures: Matsui: Pfizer: Consultancy; Bristol-Meyers Squibb: Consultancy; Infinity Phamaceuticals: Consultancy, Patents & Royalties; Merck: Consultancy, Research Funding; Geron Corporation: Research Funding.
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Yamaguchi, Masaru, Tokuhisa Hirouchi, Mitsuru Chiba, Satoru Monzen, Hironori Yoshino, Junya Ishikawa, Takakiyo Tsujiguchi, et al. "Thrombopoietin-Mimetic Romiplostim Confers the Complete Survival Rate to Mice Exposed to Lethal Ionizing Radiation." Blood 126, no. 23 (December 3, 2015): 2390. http://dx.doi.org/10.1182/blood.v126.23.2390.2390.
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Abstract Radiation-related casualties following exposure to a lethal dose of ionizing radiation show severe acute radiation syndromes (ARS) involving bone marrow death and gastrointestinal death. ARS cause decreases in red blood cell count, white blood cell count, platelet count and gastrointestinal dysfunction, finally leading to death caused by systemic bleeding. Therefore, reconstitution and restoration of hematopoiesis is a top priority. Although bone marrow transplantation (BMT) is also available for recovery from radiation-induced bone marrow damage, BMT for victims in radiation accidents has many limitations, including histocompatibility, age constraints, HLA type and the fact that immunosuppression would be required to reduce the risk of graft versus host rejection. In contrast, pharmacological approaches can accommodate a large number of victims with few limitations. Our previous study showed that the combined administration of erythropoietin, granulocytecolony stimulating factor and nandrolone decanoate after lethal ionizing irradiation resulted in the survival of approximately 50% of irradiated mice at day 30. When a c-Mpl agonist (Romiplostim: RP) was added to this protocol, 100% survival was obtained. Finally, we found that RP play a key role in the survival of irradiated mice. In the present study, we examined the effects of RP alone on mice exposed to lethal radiation. RP was administered at a dosage of 50 μg/kg of body weight/day to 8-weekold female C57BL/6JJcl mice for 1, 3, or 5 days immediately following exposure to a lethal 7 Gy dose of 137Cs γ-rays. The condition of each animal was analyzed via morphological evaluations of the small intestine and various parameters such as the numbers of peripheral blood cells, bone marrow cells, and hematopoietic progenitor cells along with cell surface antigen expression. By day 30, all untreated irradiated control mice died, whereas RP administration for 3 or 5 consecutive days after irradiation led to a 100% survival rate among the irradiated mice. At this time, the numbers of peripheral blood cells, bone marrow cells and hematopoietic progenitor cells were not significantly different between RP-untreated non-irradiated and RP-treated irradiated mice. In addition, the expression of macrophages, granulocytes and erythroid progenitors-related cell surface antigens on the bone marrow cells was significantly recovered in RP-treated irradiated mice compared to RP-untreated irradiated mice until day 20 after γ-irradiation. And, to estimate the effects of RP on gastrointestinal tissues in each individual, morphological evaluation H&E stain of the small intestine was performed until day 20 after γ-irradiation. As a result, RP promoted the recovery of gastrointestinal tissues damages in RP-treated irradiated mice compared to RP-untreated irradiated mice. Regarding cell death, radiation-induced gamma-H2AX expression in the nuclear of bone marrow cell was significantly decreased in RP-treated irradiated mice compared to RP-untreated irradiated mice immediately and after a period of 24 hours following a lethal 7 Gy dose of X-irradiation, indicating that the rate of apoptotic bone marrow cells was significantly decreased by RP-treatment. Meanwhile, 53BP1, which is well known as non-homologous end joining (NHEJ) factor, was significantly increased, showing that RP promoted NHEJ DNA repair in bone marrow cells treated with RP. These results demonstrate that c-Mpl agonist RP promotes the recovery of serious damages caused by lethal irradiation to the hematopoietic and gastrointestinal systems, and RP might be a useful radiomitigator in the case of ARS. Disclosures No relevant conflicts of interest to declare.
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Altman, K. I., H. M�hlensiepen, R. Wolters, O. Muzik, and L. E. Feinendegen. "Rubidium transport in irradiated vitamin-E-deficient bone marrow cells." Radiation and Environmental Biophysics 32, no. 1 (March 1993): 59–64. http://dx.doi.org/10.1007/bf01213131.
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Murakami, Sho, Hironori Yoshino, Junya Ishikawa, Masaru Yamaguchi, Takakiyo Tsujiguchi, Ayaka Nishiyama, Kouki Yokoyama, and Ikuo Kashiwakura. "Effects of ionizing radiation on differentiation of murine bone marrow cells into mast cells." Journal of Radiation Research 56, no. 6 (October 8, 2015): 865–71. http://dx.doi.org/10.1093/jrr/rrv061.
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Chun, Sung Hak, Ga-Young Park, Yu Kyeong Han, Sung Dae Kim, Joong Sun Kim, Chang Geun Lee, and Kwangmo Yang. "Effect of Low dose Radiation on Differentiation of Bone Marrow Cells into Dendritic Cells." Dose-Response 11, no. 3 (September 29, 2012): dose—response.1. http://dx.doi.org/10.2203/dose-response.12-041.lee.
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Wierenga, Pieter K., Isabelle Lombaert, Willy Visser, Harm H. Kampinga, Gerald de Haan, and Rob P. Coppes. "Bone Marrow-Derived Stem Cells Reduce Radiation-Induced Damage to Salivary Glands." Blood 104, no. 11 (November 16, 2004): 1194. http://dx.doi.org/10.1182/blood.v104.11.1194.1194.
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Abstract The salivary glands are often included in the field of irradiation during radiotherapy of head and neck cancer. This can result in severe side-effects that reduces the quality of life of the patient and may even limit the treatment dose. Late damage to the salivary glands is mainly caused by exhaustion of the tissue specific stem cells. Post-irradiation replacement of salivary gland stem cells with donor stem cells may ameliorate radiation-induced complications. Bone marrow-derived stem cells (BMSC) have been shown to be multipotent and thereby able to engraft in many tissues after injury. In this study, we assessed the potential of BMSC to reduce irradiation-induced salivary gland damage. C57BL/6 mice were transplanted with bone marrow from eGFP transgenic animals. After two months the salivary glands of these chimeric mice were locally irradiated with 15 Gy. BMSC were mobilized 10, 30 and/or 60 days after irradiation by s.c. injection of rHu-PEG-G-CSF. Saliva secretion (μl/15 minutes) was measured up to 90 days after irradiation by pilocarpine induction. Hereafter, the glands were extirpated and examined for eGFP-expression. From every individual animal one parotid and one submandibular gland was used to prepare single cell suspensions in order to detect eGFP-positve cells by flow cytometry. The other parotid and submandibular glands were analyzed using confocal laser fluorescence scanning microscopy and light microscopy. G-CSF treatment yielded in an increase of saliva flow for all time points. The optimal time-point for mobilization, however, was 30 days after irradiation as is demonstrated by an improvement of salivary flow from 5 to 30% when compared to radiation alone. FACS analysis showed that up to 10% of the isolated cells were eGFP-positive. Microscopic analysis revealed a similar amount of positive cells and an improved morphology. Immuno-histochemistry using anti-SM-actin antibodies showed the close vicinity of actin and eGFP within the cells, demonstrating the occurence of BMSC derived myoepithelial cells in irradiated salivary glands. Furthermore, using cell-type specific antibodies, the meyoepethilial nature of the eGFP positive was revealed. In conclusion, the results show that BMSC home to severely damaged salivary glands after mobilization. Hence, BMSC mobilization could become a promising modality to ameliorate radiation-induced complications in salivary glands after radiotherapy.
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Dong, Xian-Zhe, Yu-Ning Wang, Xiao Tan, Ping Liu, Dai-Hong Guo, and Can Yan. "Protective Effect of JXT Ethanol Extract on Radiation-Induced Hematopoietic Alteration and Oxidative Stress in the Liver." Oxidative Medicine and Cellular Longevity 2018 (October 28, 2018): 1–12. http://dx.doi.org/10.1155/2018/9017835.
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This study aims at investigating the radioprotective effect of ethanol extract from Ji-Xue-Teng (JXT,Spatholobus suberectus) on radiation-induced hematopoietic alteration and oxidative stress in the liver. Mice were exposed to a single acuteγ-radiation for the whole body at the dose of 6.0 Gy, then subjected to administration of amifostine (45 mg/kg) or JXT (40 g crude drug/kg) once a day for 28 consecutive days, respectively. Bone marrow cells and hemogram including white cells, red cells, platelet counts, and hemoglobin level were examined. The protein expression levels of pJAK2/JAK2, pSTAT5a/STAT5a, pSTAT5b/STAT5b, and Bcl-2 in bone marrow tissue; levels of reactive oxygen species (ROS); and the activity of superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH-Px) in serum and liver tissue were determined. At the end of the experiment, the effect of JXT on cell viability and G-CSF and G-CSFR levels in NFS-60 cells were tested by CCK-8 assay, ELISA, and flow cytometry. The results showed that the mice exposed toγ-radiation alone exhibited a typical hematopoietic syndrome. In contrast, at the end of the 28-day experiment, irradiated mice subjected to oral administration of JXT showed an obvious improvement on blood profile with reduced leucopenia, thrombocytopenia (platelet counts), RBC, and hemoglobin levels, as well as bone marrow cells. The expression of pJAK2/JAK2, pSTAT5a/STAT5a, and Bcl-2 in bone marrow tissue was increased after JXT treatment. The elevation of ROS was due to radiation-induced toxicity, but JXT significantly reduced the ROS level in serum and liver tissue, elevated endogenous SOD and GSH-PX levels, and reduced the MDA level in the liver. JXT could also increase cell viability and G-CSFR level in NFS-60 cells, which was similar to exogenous G-CSF. Our findings suggested that oral administration of JXT effectively facilitated the recovery of hematopoietic bone marrow damage and oxidative stress of the mice induced byγ-radiation.
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Sasi, Sharath P., Daniel Park, Sujatha Muralidharan, Justin Wage, Albert Kiladjian, Jillian Onufrak, Heiko Enderling, Xinhua Yan, and David A. Goukassian. "Particle Radiation-Induced Nontargeted Effects in Bone-Marrow-Derived Endothelial Progenitor Cells." Stem Cells International 2015 (2015): 1–15. http://dx.doi.org/10.1155/2015/496512.
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Bone-marrow- (BM-) derived endothelial progenitor cells (EPCs) are critical for endothelial cell maintenance and repair. During future space exploration missions astronauts will be exposed to space irradiation (IR) composed of a spectrum of low-fluence protons (1H) and high charge and energy (HZE) nuclei (e.g., iron-56Fe) for extended time. How the space-type IR affects BM-EPCs is limited. In media transfer experimentsin vitrowe studied nontargeted effects induced by1H- and56Fe-IR conditioned medium (CM), which showed significant increase in the number of p-H2AX foci in nonirradiated EPCs between 2 and 24 h. A 2–15-fold increase in the levels of various cytokines and chemokines was observed in both types of IR-CM at 24 h.Ex vivoanalysis of BM-EPCs from single, low-dose, full-body1H- and56Fe-IR mice demonstrated a cyclical (early 5–24 h and delayed 28 days) increase in apoptosis. This early increase in BM-EPC apoptosis may be the effect of direct IR exposure, whereas late increase in apoptosis could be a result of nontargeted effects (NTE) in the cells that were not traversed by IR directly. Identifying the role of specific cytokines responsible for IR-induced NTE and inhibiting such NTE may prevent long-term and cyclical loss of stem and progenitors cells in the BM milieu.
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Carsten, Ronald E., Annette M. Bachand, Susan M. Bailey, and Robert L. Ullrich. "Resveratrol Reduces Radiation-Induced Chromosome Aberration Frequencies in Mouse Bone Marrow Cells." Radiation Research 169, no. 6 (June 2008): 633–38. http://dx.doi.org/10.1667/rr1190.1.
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Vegesna, W. H. McBride, V. "The role of T-cells in radiation pneumonitis after bone marrow transplantation." International Journal of Radiation Biology 76, no. 4 (January 2000): 517–21. http://dx.doi.org/10.1080/095530000138529.
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EMMONS, RUSSELL, MATTHEW NGU, GUANYING XU, DIEGO HERNÁNDEZ-SAAVEDRA, HONG CHEN, and MICHAEL DE LISIO. "Effects of Obesity and Exercise on Bone Marrow Progenitor Cells after Radiation." Medicine & Science in Sports & Exercise 51, no. 6 (June 2019): 1126–36. http://dx.doi.org/10.1249/mss.0000000000001894.
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Farooqi, Zeba, and P. C. Kesavan. "Low-dose radiation-induced adaptive response in bone marrow cells of mice." Mutation Research Letters 302, no. 2 (June 1993): 83–89. http://dx.doi.org/10.1016/0165-7992(93)90008-j.
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Goff, Julie P., Tracy M. Dixon, Michael W. Epperly, Melissa Sprachman, Peter Wipf, Xichen Zhang, and Joel S. Greenberger. "Serial Imaging of Luciferase Positive Bone Marrow Stromal Cell Migration to Form Radiation Pulmonary Fibrosis." Blood 120, no. 21 (November 16, 2012): 4734. http://dx.doi.org/10.1182/blood.v120.21.4734.4734.
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Abstract Abstract 4734 Thoracic irradiation of C57BL/6 mice leads to an acute reaction phase in the lungs characterized by increased cytokine production and inflammation days 1–14 post irradiation. This is followed by a latent period where inflammation, histologic appearance and cytokine response returns to control levels. The late reaction phase occurs 100+ days post irradiation and is characterized by organizing alveolitis/fibrosis and involves migration of marrow origin macrophages and proliferating mesenchymal stem cells (fibroblasts), a subpopulation which migrates from marrow to the lungs. To quantitate migration in real time, thoracic irradiated mice were either made chimeric for luciferase positive (luc+) whole marrow or were injected with cells from a positive luc+ bone marrow stromal cell line and serially imaged at day 7, 60 or 120 using an IVIS.. 200 Optical Imaging System. As a control for migration to the lung, another group of mice received 20Gy to the right hind leg and 1.5 ×106 luc+ bone marrow stromal cells i.p. Imaging of chimeric mice revealed luc+ cell lung migration only after day 120. C57BL/6NTac female mice that received 20Gy thoracic irradiation followed by an i.p. injection 1.5 × 106 luc+ positive bone marrow stromal cells revealed no migration of luc+ cells to the lungs at day 7 or day 60. Furthermore there was no migration to 20Gy irradiated leg at any timepoint. In marked contrast, at the time of the late reaction phase, at day 100, fibrosis was revealed as an increase in luc+ cell migration in lungs. The lung fibrosis model in C57BL/6 mice combined with live imaging allows sequential measurement of the effect of agents which may alter migration of bone marrow cells that contribute to radiation pulmonary fibrosis. Disclosures: No relevant conflicts of interest to declare.
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Lieberman, M., G. A. Hansteen, J. M. McCune, M. L. Scott, J. H. White, and I. L. Weissman. "Indirect induction of radiation lymphomas in mice. Evidence for a novel, transmissible leukemogen." Journal of Experimental Medicine 166, no. 6 (December 1, 1987): 1883–93. http://dx.doi.org/10.1084/jem.166.6.1883.
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The transmission of a lymphomagenic agent(s) from the bone marrow of irradiated mice to thymic target cells has been demonstrated by: (a) the induction of T cell lymphomas in nonirradiated thymic grafts implanted in irradiated, Thy-l-congenic mice, (b) the induction of T cell lymphomas of host origin in mice infused with bone marrow from irradiated, Thy-l-congenic donors. The latter procedure also yields an appreciable number of pre-B cell lymphomas of uncertain origin. The results confirm Kaplan's theory that radiation induces thymic lymphomas in mice by an indirect mechanism. However, the previously described radiation leukemia virus is clearly not involved in the majority of transferred lymphomas. We propose that the mediating agent in radiation lymphomagenesis is a novel, transmissible agent induced in the bone marrow, but exerting its transforming activity on cells in the thymus. The nature and mode of action of the agent are under investigation.
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Greenberger, Joel S., Pervin Anklesaria, Jean Leif, Maryann Sakakeeny, Debra English, Kenneth Kase, Indra Das, Christine Buckley, and T. J. Fitzgerald. "Indirect gamma irradiation leukemogenesis through bone marrow stromal cells." International Journal of Radiation Oncology*Biology*Physics 21 (January 1991): 187–88. http://dx.doi.org/10.1016/0360-3016(91)90565-l.
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Chen, Yong Feng, Zhong Min Wu, Cong Xie, Shi Bai, and Li Dong Zhao. "Expression Level of IL-6 Secreted by Bone Marrow Stromal Cells in Mice with Aplastic Anemia." ISRN Hematology 2013 (June 18, 2013): 1–6. http://dx.doi.org/10.1155/2013/986219.
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Parasecretion of the hematopoietic cytokines is considered as one of the mechanisms account for bone marrow hematopoiesis disorder. In this study, the level of IL-6 secreted by bone marrow stromal cells from a mouse model of aplastic anemia was analyzed. The aplastic anemia mouse model was established with cyclophosphamide in combination with chloramphenicol and 60Coγ radiation. The impairment of bone marrow hematopoiesis induced by irradiation and chemotherapeutic drugs was subsequently characterized by peripheral blood cell count, pathomorphological changes, and apoptosis rate. Furthermore, the in vitro proliferation of bone marrow stromal cells (BMSC) and the IL-6 secretion levels of BMSC were analyzed. In our model of aplastic anemia, the number of peripheral blood cells and bone marrow cells (BMC) were notably decreased, and the apoptosis rate of BMC increased. Furthermore, the proliferation of BMSC was obviously impeded while the IL-6 secretion levels of BMSC significantly increased. The findings of our study suggested that the IL-6 secretion level may be enhanced to some extent by the induction of aplastic anemia caused by irradiation and chemotherapeutic drugs and that the abnormal level of IL-6 might probably interfere with the stability of the bone marrow hematopoietic microenvironment.
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Muramoto, Garrett G., Benny Chen, Xiuyu Cui, and John Chute. "Endothelial Cells Mediate the Repair of Human Bone Marrow Stem and Progenitor Cells Following Radiation Injury." Blood 104, no. 11 (November 16, 2004): 2341. http://dx.doi.org/10.1182/blood.v104.11.2341.2341.
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Abstract The purposeful misuse of ionizing radiation has been recognized as a major bioterrorism threat in the United States. Although the myeloablative effects of ionizing radiation exposure have been well established, definitive treatments for potential victims of radiation injury are lacking. We have recently demonstrated that BM stem cells can be harvested from mice following exposure to lethal dose total body irradiation and can subsequently recover multilineage repopulating potential via ex vivo culture with microvascular endothelial cells (EC). However, it remains to be determined whether human hematopoietic stem cells (HSC) can be recovered in a similar manner following high dose radiation injury. In this study, we examined the capacity for ex vivo culture with and without primary human endothelial cells to support the cellular repair and recovery of primary human BM CD34+ cells following exposure to high dose irradiation. Exposure of primary BM CD34+ cells to 400 cGy resulted in a 40% decline in total viable cells and an 89% decline in CD34+CD38− cells compared to input despite 10 day culture with optimal concentrations of thrombopoietin, stem cell factor, and flt-3 ligand alone. Conversely, co-culture of 400 cGy irradiated BM CD34+ cells with primary human brain endothelial cells (LS-01) resulted in a 6-fold and 22-fold increase in total cells and CD34+CD38− cells compared to input, respectively. Non-contact cultures with LS-01 resulted in comparable recovery of total cells and the CD34+CD38− subset by 10 days. Concordantly, TSF-cultured progeny contained 5-fold greater numbers of early apoptotic and necrotic cells within the total and CD34+CD38− fractions as compared to the progeny of contact and non-contact endothelial cultures. Colony forming cell (CFC) assays demonstrated that 400 cGy exposure caused an 8-fold reduction in CFU-total compared to normal BM CD34+ cells and no recovery of CFU-GM, BFU-E, or CFU-Mix was observed following TSF culture. Co-culture with LS-01 resulted in the recovery of 50% of CFU-total compared to normal BM CD34+ cells. In order to assess HSC content post-irradiation, NOD/SCID mice were transplanted with normal BM CD34+ cells, 400 cGy irradiated BM CD34+ cells, and the progeny of 400 cGy irradiated cells following ex vivo culture. 100% of mice transplanted with normal BM CD34+ cells (7.5 x 105) demonstrated human hematopoietic engraftment at 6 weeks, whereas 0% of mice transplanted with 400 cGy irradiated BM CD34+ cells showed detectable human repopulation. Twenty-five percent of mice transplanted with 400 cGy irradiated/LS-01 cultured cells demonstrated human repopulation, whereas 0% of mice transplanted with 400 cGy irradiated/TSF-cultured cells showed human engraftment. These data demonstrate that ionizing radiation has a profoundly toxic effect on both human HSC and committed progenitor cells. Endothelial cells and endothelial cell-derived soluble factors appear to provide anti-apoptotic signals to BM progenitor cells following radiation damage, allowing cellular repair of committed progenitors as well as cells with in vivo repopulating capacity. Cytokine combinations alone, such as TSF, appear ineffective toward rescuing human BM stem/progenitor cells from radiation damage. Studies are ongoing to optimize the application of endothelial cells and endothelial cell-derived growth factors to stimulate HSC repair following radiation injury.
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Chailakhyan, R. K., V. I. Yusupov, Yu F. Gorskaya, A. I. Kuralesova, Yu V. Gerasimov, A. P. Sviridov, A. Kh Tambiev, et al. "Effect of acoustic pulses and EHF radiation on multipotent marrow stromal cells in tissue engineering constructs." Journal of Innovative Optical Health Sciences 10, no. 01 (January 2017): 1650036. http://dx.doi.org/10.1142/s179354581650036x.
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In this paper, we studied the effects of physical factors, such as, acoustic pulses of laser-induced hydrodynamics (ALIH) and extremely-high frequencies (EHF) radiation, on the formation of heterotopic bone marrow organs. A suspension of precipitated bone marrow cells from CBA mice were exposed to ALIH pulses and EHF radiation separately and in their combination tissue engineering constructs, presenting gelatin sponges 2 by 2 by 2[Formula: see text]mm in size containing 107 nucleated bone marrow cells, were exposed to physical factors and were implanted under the renal capsules of syngeneic mice. The newly formed hematopoietic organs were examined in three and five months later after treatment. The five months old transplants were bigger in size than the three months old transplants. The number of hematopoietic cells in the rest of the groups increased during this period by a factor from 3 to 10, the increase being as high as 20-fold in the ALIH[Formula: see text]EHF group. Maximal concentration of multipotent stromal cells (MSCs) was in the EHF[Formula: see text]ALIH, and minimal concentration was in the ALIH[Formula: see text]EHF. The accumulation rate of bone capsule weight was highest for the transplants of EHF[Formula: see text]ALIH and ALIH-sponge groups during the first three months. These data showed that the combined impact of the EHF[Formula: see text]ALIH on MSCs is the most effective for the formation of bone marrow transplantation.
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Cary, Lynnette, Daniel Noutai, Rudolph Salber, Opeyemi Fadiyimu, Arthur Gross, Graca Almeida-Porada, Yared Kidane, and Mark Whitnall. "Bone Marrow Endothelial Cells Influence Function and Phenotype of Hematopoietic Stem and Progenitor Cells after Mixed Neutron/Gamma Radiation." International Journal of Molecular Sciences 20, no. 7 (April 11, 2019): 1795. http://dx.doi.org/10.3390/ijms20071795.
Full textAbstract:
The bone marrow (BM) microenvironment plays a crucial role in the maintenance and regeneration of hematopoietic stem (HSC) and progenitor cells (HSPC). In particular, the vascular niche is responsible for regulating HSC maintenance, differentiation, and migration of cells in and out of the BM. Damage to this niche upon exposure to ionizing radiation, whether accidental or as a result of therapy, can contribute to delays in HSC recovery and/or function. The ability of BM derived-endothelial cells (BMEC) to alter and/or protect HSPC after exposure to ionizing radiation was investigated. Our data show that exposure of BMEC to ionizing radiation resulted in alterations in Akt signaling, increased expression of PARP-1, IL6, and MCP-1, and decreased expression of MMP1 and MMP9. In addition, global analysis of gene expression of HSC and BMEC in response to mixed neutron/gamma field (MF) radiation identified 60 genes whose expression was altered after radiation in both cell types, suggesting that a subset of genes is commonly affected by this type of radiation. Focused gene analysis by RT-PCR revealed two categories of BMEC alterations: (a) a subset of genes whose expression was altered in response to radiation, with no additional effect observed during coculture with HSPC, and (b) a subset of genes upregulated in response to radiation, and altered when cocultured with HSPC. Coculture of BMEC with CD34+ HSPC induced HSPC proliferation, and improved BM function after MF radiation. Nonirradiated HSPC exhibited reduced CD34 expression over time, but when irradiated, they maintained higher CD34 expression. Nonirradiated HSPC cocultured with nonirradiated BMEC expressed lower levels of CD34 expression compared to nonirradiated alone. These data characterize the role of each cell type in response to MF radiation and demonstrate the interdependence of each cell’s response to ionizing radiation. The identified genes modulated by radiation and coculture provide guidance for future experiments to test hypotheses concerning specific factors mediating the beneficial effects of BMEC on HSPC. This information will prove useful in the search for medical countermeasures to radiation-induced hematopoietic injury.
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Mulyani, Sri Wigati Mardi, Eha Renwi Astuti, Otty Ratna Wahyuni, Diah Savitri Ernawati, and Nastiti Faradilla Ramadhani. "Xerostomia Therapy Due to Ionized Radiation Using Preconditioned Bone Marrow-Derived Mesenchymal Stem Cells." European Journal of Dentistry 13, no. 02 (May 2019): 238–42. http://dx.doi.org/10.1055/s-0039-1694697.
Full textAbstract:
Abstract Objectives The aim of this study was to describe the process of regeneration of damaged salivary glands due to ionizing radiations by bone marrow mesenchymal stem cells (BM-MSCs) transplantation that have been given hypoxic preconditioning with 1% O2 concentration. Materials and Methods Stem cell culture was performed under normoxic (O2: 21%) and hypoxic conditions by incubating the cells for 48 hours in a low oxygen tension chamber consisting of 95% N2, 5% CO2, and 1% O2. Thirty male Wistar rats were divided into four groups: two groups of control and two groups of treatment. A single dose of 15 Gy radiation was provided to the ventral region of the neck in all treatment groups, damaging the salivary glands. BM-MSCs transplantation was performed in the treatment groups for normoxia and hypoxia 24-hour postradiation. Statistical Analysis Statistical analysis was done using normality test, followed by MANOVA test (p < 0.05). Results There was a significant difference in the expression of binding SDF1-CXCR4, Bcl-2 (p < 0.05) and also the activity of the enzyme α-amylase in all groups of hypoxia. Conclusion BM-MSCs transplantation with hypoxic precondition increases the expression of binding SDF1-CXCR4, Bcl-2 that contributes to cell migration, cell survival, and cell differentiation.
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Zuckerman, KS, CW Prince, and M. Ribadeneira. "Sl/Sld mouse bone marrow stroma in vitro contains an active radiation- sensitive inhibitor of normal hemopoiesis." Blood 68, no. 6 (December 1, 1986): 1201–6. http://dx.doi.org/10.1182/blood.v68.6.1201.1201.
Full textAbstract:
Abstract Sl/Sld mice have a defective hemopoietic microenvironment. It has been assumed, based upon previous studies, that the primary abnormality in these mice is simply lack of a necessary supportive or inductive material within the hemopoietic stroma. We used in vitro long-term bone marrow cultures to characterize further the nature of the hemopoietic microenvironmental defect in Sl/Sld mice. Sl/Sld mouse bone marrow cells consistently produced less than 10% of the total hemopoietic cells and multipotent and unipotent hemopoietic progenitor cells produced in cultures of marrow from normal, congenic +/+ mice. If fresh Sl/Sld and +/+ marrow cells were mixed prior to establishing long-term marrow cultures, there was a direct correlation between number of Sl/Sld cells added and degree of inhibition of +/+ hemopoiesis. A pre- established, confluent Sl/Sld adherent stromal layer inhibited hemopoiesis by fresh +/+ marrow cells by nearly 70%, as compared with dishes with irradiated +/+ or no stroma. This inhibitory effect was abrogated by irradiation of the Sl/Sld stroma prior to addition of the fresh +/+ marrow cells. Similarly, unirradiated, but not 9 to 200 Gy irradiated Sl/Sld stroma inhibited proliferation of the factor- dependent FDC-P1 hemopoietic progenitor cell line. Thus, the Sl/Sld hemopoietic microenvironment actively inhibits hemopoiesis in vitro, and this inhibition can be at least partially eliminated by irradiation of the Sl/Sld stroma.
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Zuckerman, KS, CW Prince, and M. Ribadeneira. "Sl/Sld mouse bone marrow stroma in vitro contains an active radiation- sensitive inhibitor of normal hemopoiesis." Blood 68, no. 6 (December 1, 1986): 1201–6. http://dx.doi.org/10.1182/blood.v68.6.1201.bloodjournal6861201.
Full textAbstract:
Sl/Sld mice have a defective hemopoietic microenvironment. It has been assumed, based upon previous studies, that the primary abnormality in these mice is simply lack of a necessary supportive or inductive material within the hemopoietic stroma. We used in vitro long-term bone marrow cultures to characterize further the nature of the hemopoietic microenvironmental defect in Sl/Sld mice. Sl/Sld mouse bone marrow cells consistently produced less than 10% of the total hemopoietic cells and multipotent and unipotent hemopoietic progenitor cells produced in cultures of marrow from normal, congenic +/+ mice. If fresh Sl/Sld and +/+ marrow cells were mixed prior to establishing long-term marrow cultures, there was a direct correlation between number of Sl/Sld cells added and degree of inhibition of +/+ hemopoiesis. A pre- established, confluent Sl/Sld adherent stromal layer inhibited hemopoiesis by fresh +/+ marrow cells by nearly 70%, as compared with dishes with irradiated +/+ or no stroma. This inhibitory effect was abrogated by irradiation of the Sl/Sld stroma prior to addition of the fresh +/+ marrow cells. Similarly, unirradiated, but not 9 to 200 Gy irradiated Sl/Sld stroma inhibited proliferation of the factor- dependent FDC-P1 hemopoietic progenitor cell line. Thus, the Sl/Sld hemopoietic microenvironment actively inhibits hemopoiesis in vitro, and this inhibition can be at least partially eliminated by irradiation of the Sl/Sld stroma.
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Raghunathan, Kiruthiga, and Brindha Devi P. "CHIMERIC ANTIGEN RECEPTOR FOR CHRONIC LYMPHOCYTIC LEUKEMIA - A REVIEW." Asian Journal of Pharmaceutical and Clinical Research 12, no. 1 (January 7, 2019): 62. http://dx.doi.org/10.22159/ajpcr.2018.v12i1.29642.
Full textAbstract:
Chronic lymphocytic leukemia cancer is a deadly one which affects the bone marrow from making it to produce more amounts of white blood cells in the humans. This disease can be treated either by radiation therapy, bone marrow transplantation, chemotherapy, or immunotherapy. In radiation therapy, the ionizing radiation is used toward the tumor cells, but the main drawback is the radiation may affect the normal cells as well. To overcome this drawback, immunotherapy chimeric antigen receptor (CAR) is used. These CAR cells will target only the antigen of the tumor cells and not damage the normal cells in the body. In this therapy, the T-cells are taken either from the patients or a healthy donor and are engineered to express the CARs which are called as CAR-T-cells. When these CAR-T-cells come in contact with the antigen present on the surface of the tumor cells, they will get activated and become toxic to the tumor cells. This new class of therapy is having a great prospect in cancer immunotherapy.
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Raghunathan, Kiruthiga, and Brindha Devi P. "CHIMERIC ANTIGEN RECEPTOR FOR CHRONIC LYMPHOCYTIC LEUKEMIA - A REVIEW." Asian Journal of Pharmaceutical and Clinical Research 12, no. 1 (January 7, 2019): 62. http://dx.doi.org/10.22159/ajpcr.2019.v12i1.29642.
Full textAbstract:
Chronic lymphocytic leukemia cancer is a deadly one which affects the bone marrow from making it to produce more amounts of white blood cells in the humans. This disease can be treated either by radiation therapy, bone marrow transplantation, chemotherapy, or immunotherapy. In radiation therapy, the ionizing radiation is used toward the tumor cells, but the main drawback is the radiation may affect the normal cells as well. To overcome this drawback, immunotherapy chimeric antigen receptor (CAR) is used. These CAR cells will target only the antigen of the tumor cells and not damage the normal cells in the body. In this therapy, the T-cells are taken either from the patients or a healthy donor and are engineered to express the CARs which are called as CAR-T-cells. When these CAR-T-cells come in contact with the antigen present on the surface of the tumor cells, they will get activated and become toxic to the tumor cells. This new class of therapy is having a great prospect in cancer immunotherapy.
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Casamassima, F., C. Ruggiero, D. Caramella, E. Tinacci, N. Villari, and M. Ruggiero. "Hematopoietic bone marrow recovery after radiation therapy: MRI evaluation." Blood 73, no. 6 (May 1, 1989): 1677–81. http://dx.doi.org/10.1182/blood.v73.6.1677.1677.
Full textAbstract:
Abstract Magnetic resonance imaging (MRI) is able to detect the increase of adipocytes in the hematopoietic bone marrow that occurs as a consequence of radiotherapy and is indicative of the loss of myeloid tissue. By monitoring this process, it is also possible to determine the recovery of the bone marrow. The amount of viable hematopoietic tissue plays a fundamental role in determining whether the patient is able to undergo further antineoplastic therapy, particularly chemotherapy. We examined 35 patients who had been treated with radiotherapy for Hodgkin's lymphoma (12), uterine cervix carcinoma (nine), ovarian dysgerminoma (six), testicular seminoma (four), and non- Hodgkin's lymphoma (four). We observed that radiation-induced modifications of the MRI pattern in the bone marrow are tightly linked to two parameters; the administered radiation dose and the length of time passed after the treatment. Bone marrow recovery was observed only when patients were treated with doses lower than 50 Gy. The earlier radiation-induced modifications of the bone marrow MRI pattern occurred 6 to 12 months after irradiation, and they were most evident 5 to 6 years after the treatment. From 2 to 9 years after radiotherapy, we observed partial recovery. Complete recovery, when it occurred, was observed only 10 to 23 years after the treatment. Our results indicate that MRI studies are likely to be useful in the assessment of radiation- induced injuries.