Journal articles: 'Mesenchynol stronel cels'

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Srinivas, Ampati. "The Constantly Highly Expression of Limbal Stromal Cells Compared to the Bone Marrow Mesenchymal Stromal Cells, Adipose-Derived Mesenchymal Stromal Cells and Foreskin Fibroblasts." Stem Cells Research and Therapeutics International 1, no. 1 (April 16, 2019): 01–06. http://dx.doi.org/10.31579/2643-1912/005.

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Tarusin, D. "ENCAPSULATION OF MESENCHYMAL STROMAL CELLS IN ALGINATE MICROSPHERES." Biotechnologia Acta 9, no. 4 (August 2016): 58–66. http://dx.doi.org/10.15407/biotech9.04.058.

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Jerkic, Mirjana, Stéphane Gagnon, Razieh Rabani, Taylor Ward-Able, Claire Masterson, Gail Otulakowski, Gerard F. Curley, John Marshall, Brian P. Kavanagh, and John G. Laffey. "Human Umbilical Cord Mesenchymal Stromal Cells Attenuate Systemic Sepsis in Part by Enhancing Peritoneal Macrophage Bacterial Killing via Heme Oxygenase-1 Induction in Rats." Anesthesiology 132, no. 1 (January 1, 2020): 140–54. http://dx.doi.org/10.1097/aln.0000000000003018.

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Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Mesenchymal stromal cells have therapeutic potential in sepsis, but the mechanism of action is unclear. We tested the effects, dose-response, and mechanisms of action of cryopreserved, xenogeneic-free human umbilical cord mesenchymal stromal cells in a rat model of fecal peritonitis, and examined the role of heme oxygenase-1 in protection. Methods Separate in vivo experiments evaluated mesenchymal stromal cells in fecal sepsis, established dose response (2, 5, and 10 million cells/kg), and the role of heme oxygenase-1 in mediating human umbilical cord–derived mesenchymal stromal/stem cell effects. Ex vivo studies utilized pharmacologic blockers and small inhibitory RNAs to evaluate mechanisms of mesenchymal stromal cell enhanced function in (rodent, healthy and septic human) macrophages. Results Human umbilical cord mesenchymal stromal cells reduced injury and increased survival (from 48%, 12 of 25 to 88%, 14 of 16, P = 0.0033) in fecal sepsis, with dose response studies demonstrating that 10 million cells/kg was the most effective dose. Mesenchymal stromal cells reduced bacterial load and peritoneal leukocyte infiltration (from 9.9 ± 3.1 × 106/ml to 6.2 ± 1.8 × 106/ml, N = 8 to 10 per group, P < 0.0001), and increased heme oxygenase-1 expression in peritoneal macrophages, liver, and spleen. Heme oxygenase-1 blockade abolished the effects of mesenchymal stromal cells (N = 7 or 8 per group). Mesenchymal stromal cells also increased heme oxygenase-1 expression in macrophages from healthy donors and septic patients. Direct ex vivo upregulation of macrophage heme oxygenase-1 enhanced macrophage function (phagocytosis, reactive oxygen species production, bacterial killing). Blockade of lipoxin A4 production in mesenchymal stromal cells, and of prostaglandin E2 synthesis in mesenchymal stromal cell/macrophage cocultures, prevented upregulation of heme oxygenase-1 in macrophages (from 9.6 ± 5.5-fold to 2.3 ± 1.3 and 2.4 ± 2.3 respectively, P = 0.004). Knockdown of heme oxygenase-1 production in macrophages ablated mesenchymal stromal cell enhancement of macrophage phagocytosis. Conclusions Human umbilical cord mesenchymal stromal cells attenuate systemic sepsis by enhancing peritoneal macrophage bacterial killing, mediated partly via upregulation of peritoneal macrophage heme oxygenase-1. Lipoxin A4 and prostaglandin E2 play key roles in the mesenchymal stromal cell and macrophage interaction.

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Varkouhi, Amir K., Mirjana Jerkic, Lindsay Ormesher, Stéphane Gagnon, Sakshi Goyal, Razieh Rabani, Claire Masterson, et al. "Extracellular Vesicles from Interferon-γ–primed Human Umbilical Cord Mesenchymal Stromal Cells Reduce Escherichia coli–induced Acute Lung Injury in Rats." Anesthesiology 130, no. 5 (May 1, 2019): 778–90. http://dx.doi.org/10.1097/aln.0000000000002655.

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Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Human umbilical cord mesenchymal stromal cells possess considerable therapeutic promise for acute respiratory distress syndrome. Umbilical cord mesenchymal stromal cells may exert therapeutic effects via extracellular vesicles, while priming umbilical cord mesenchymal stromal cells may further enhance their effect. The authors investigated whether interferon-γ–primed umbilical cord mesenchymal stromal cells would generate mesenchymal stromal cell–derived extracellular vesicles with enhanced effects in Escherichia coli (E. coli) pneumonia. Methods In a university laboratory, anesthetized adult male Sprague–Dawley rats (n = 8 to 18 per group) underwent intrapulmonary E. coli instillation (5 × 109 colony forming units per kilogram), and were randomized to receive (a) primed mesenchymal stromal cell–derived extracellular vesicles, (b) naïve mesenchymal stromal cell–derived extracellular vesicles (both 100 million mesenchymal stromal cell–derived extracellular vesicles per kilogram), or (c) vehicle. Injury severity and bacterial load were assessed at 48 h. In vitro studies assessed the potential for primed and naïve mesenchymal stromal cell–derived extracellular vesicles to enhance macrophage bacterial phagocytosis and killing. Results Survival increased with primed (10 of 11 [91%]) and naïve (8 of 8 [100%]) mesenchymal stromal cell–derived extracellular vesicles compared with vehicle (12 of 18 [66.7%], P = 0.038). Primed—but not naïve—mesenchymal stromal cell–derived extracellular vesicles reduced alveolar–arterial oxygen gradient (422 ± 104, 536 ± 58, 523 ± 68 mm Hg, respectively; P = 0.008), reduced alveolar protein leak (0.7 ± 0.3, 1.4 ± 0.4, 1.5 ± 0.7 mg/ml, respectively; P = 0.003), increased lung mononuclear phagocytes (23.2 ± 6.3, 21.7 ± 5, 16.7 ± 5 respectively; P = 0.025), and reduced alveolar tumor necrosis factor alpha concentrations (29 ± 14.5, 35 ± 12.3, 47.2 ± 6.3 pg/ml, respectively; P = 0.026) compared with vehicle. Primed—but not naïve—mesenchymal stromal cell–derived extracellular vesicles enhanced endothelial nitric oxide synthase production in the injured lung (endothelial nitric oxide synthase/β-actin = 0.77 ± 0.34, 0.25 ± 0.29, 0.21 ± 0.33, respectively; P = 0.005). Both primed and naïve mesenchymal stromal cell–derived extracellular vesicles enhanced E. coli phagocytosis and bacterial killing in human acute monocytic leukemia cell line (THP-1) in vitro (36.9 ± 4, 13.3 ± 8, 0.1 ± 0.01%, respectively; P = 0.0004) compared with vehicle. Conclusions Extracellular vesicles from interferon-γ–primed human umbilical cord mesenchymal stromal cells more effectively attenuated E. coli–induced lung injury compared with extracellular vesicles from naïve mesenchymal stromal cells, potentially via enhanced macrophage phagocytosis and killing of E. coli.

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Masterson, Claire, James Devaney, Shahd Horie, Lisa O’Flynn, Laura Deedigan, Steve Elliman, Frank Barry, Timothy O’Brien, Daniel O’Toole, and John G. Laffey. "Syndecan-2–positive, Bone Marrow–derived Human Mesenchymal Stromal Cells Attenuate Bacterial-induced Acute Lung Injury and Enhance Resolution of Ventilator-induced Lung Injury in Rats." Anesthesiology 129, no. 3 (September 1, 2018): 502–16. http://dx.doi.org/10.1097/aln.0000000000002327.

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Abstract What We Already Know about This Topic What This Article Tells Us That Is New Background Human mesenchymal stromal cells demonstrate promise for acute respiratory distress syndrome, but current studies use highly heterogenous cell populations. We hypothesized that a syndecan 2 (CD362)–expressing human mesenchymal stromal cell subpopulation would attenuate Escherichia coli–induced lung injury and enhance resolution after ventilator-induced lung injury. Methods In vitro studies determined whether CD362+ human mesenchymal stromal cells could modulate pulmonary epithelial inflammation, wound healing, and macrophage phagocytosis. Two in vivo rodent studies determined whether CD362+ human mesenchymal stromal cells attenuated Escherichia coli–induced lung injury (n = 10/group) and enhanced resolution of ventilation-induced injury (n = 10/group). Results CD362+ human mesenchymal stromal cells attenuated cytokine-induced epithelial nuclear factor kappa B activation, increased epithelial wound closure, and increased macrophage phagocytosis in vitro. CD362+ human mesenchymal stromal cells attenuated Escherichia coli–induced injury in rodents, improving arterial oxygenation (mean ± SD, 83 ± 9 vs. 60 ± 8 mmHg, P < 0.05), improving lung compliance (mean ± SD: 0.66 ± 0.08 vs. 0.53 ± 0.09 ml · cm H2O−1, P < 0.05), reducing bacterial load (median [interquartile range], 1,895 [100–3,300] vs. 8,195 [4,260–8,690] colony-forming units, P < 0.05), and decreasing structural injury compared with vehicle. CD362+ human mesenchymal stromal cells were more effective than CD362− human mesenchymal stromal cells and comparable to heterogenous human mesenchymal stromal cells. CD362+ human mesenchymal stromal cells enhanced resolution after ventilator-induced lung injury in rodents, restoring arterial oxygenation (mean ± SD: 113 ± 11 vs. 89 ± 11 mmHg, P < 0.05) and lung static compliance (mean ± SD: 0.74 ± 0.07 vs. 0.45 ± 0.07 ml · cm H2O−1, P < 0.05), resolving lung inflammation, and restoring histologic structure compared with vehicle. CD362+ human mesenchymal stromal cells efficacy was at least comparable to heterogenous human mesenchymal stromal cells. Conclusions A CD362+ human mesenchymal stromal cell population decreased Escherichia coli–induced pneumonia severity and enhanced recovery after ventilator-induced lung injury.

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Westman, Amanda M., Rachel L. Goldstein, Gino Bradica, Scott M. Goldman, Mark A. Randolph, Joseph P. Gaut, Joseph P. Vacanti, and David M. Hoganson. "Decellularized extracellular matrix microparticles seeded with bone marrow mesenchymal stromal cells for the treatment of full-thickness cutaneous wounds." Journal of Biomaterials Applications 33, no. 8 (January 16, 2019): 1070–79. http://dx.doi.org/10.1177/0885328218824759.

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Extracellular matrix materials mechanically dissociated into submillimeter particles have a larger surface area than sheet materials and enhanced cellular attachment. Decellularized porcine mesothelial extracellular matrix microparticles were seeded with bone marrow-derived mesenchymal stromal cells and cultured in a rotating bioreactor. The mesenchymal stromal cells attached and grew to confluency on the microparticles. The cell-seeded microparticles were then encapsulated in varying concentrations of fibrin glue, and the cells migrated rapidly off the microparticles. The combination of microparticles and mesenchymal stromal cells was then applied to a splinted full-thickness cutaneous in vivo wound model. There was evidence of increased cell infiltration and collagen deposition in mesenchymal stromal cells-treated wounds. Cell-seeded microparticles have potential as a cell delivery and paracrine therapy in impaired healing environments.

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Lee, Rebecca, Nicoletta Del Papa, Martin Introna, Charles F. Reese, Marina Zemskova, Michael Bonner, Gustavo Carmen-Lopez, Kristi Helke, Stanley Hoffman, and Elena Tourkina. "Adipose-derived mesenchymal stromal/stem cells in systemic sclerosis: Alterations in function and beneficial effect on lung fibrosis are regulated by caveolin-1." Journal of Scleroderma and Related Disorders 4, no. 2 (January 25, 2019): 127–36. http://dx.doi.org/10.1177/2397198318821510.

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The potential value of mesenchymal stromal/stem cell therapy in treating skin fibrosis in scleroderma (systemic sclerosis) and of the caveolin-1 scaffolding domain peptide in treating lung, skin, and heart fibrosis is known. To understand how these observations may relate to differences between mesenchymal stromal/stem cells from healthy subjects and subjects with fibrosis, we have characterized the fibrogenic and adipogenic potential of adipose-derived mesenchymal stromal/stem cells from systemic sclerosis patients, from mice with fibrotic lung and skin disease induced by systemic bleomycin treatment, and from healthy controls. Early passage systemic sclerosis adipose-derived mesenchymal stromal/stem cells have a profibrotic/anti-adipogenic phenotype compared to healthy adipose-derived mesenchymal stromal/stem cells (low caveolin-1, high α-smooth muscle actin, high HSP47, low pAKT, low capacity for adipogenic differentiation). This phenotype is mimicked by treating healthy adipose-derived mesenchymal stromal/stem cells with transforming growth factor beta or caveolin-1 small interfering RNA and is reversed in systemic sclerosis adipose-derived mesenchymal stromal/stem cells by treatment with caveolin-1 scaffolding domain peptide, but not scrambled caveolin-1 scaffolding domain peptide. Similar results were obtained with adipose-derived mesenchymal stromal/stem cells from systemic sclerosis patients and from bleomycin-treated mice, indicating the central role of caveolin-1 in mesenchymal stromal/stem cell differentiation in fibrotic disease.

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Ratushnyy, A. Yu, and L. B. Buravkova. "Cell Senescence and Mesenchymal Stromal Cells." Human Physiology 46, no. 1 (January 2020): 85–93. http://dx.doi.org/10.1134/s0362119720010132.

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Ayala-Grosso, Carlos, Rosalinda Pieruzzini, Leslie Vargas-Saturno, and José E. Cardier. "Human olfactory mesenchymal stromal cells co-expressing horizontal basal and ensheathing cell proteins in culture." Biomédica 40, no. 1 (March 1, 2020): 72–88. http://dx.doi.org/10.7705/biomedica.4762.

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Introduction: The olfactory neuro-epithelium has an intrinsic capability of renewal during lifetime provided by the existence of globose and horizontal olfactory precursor cells. Additionally, mesenchymal stromal olfactory cells also support the homeostasis of the olfactory mucosa cell population. Under in vitro culture conditions with Dulbecco modified eagle/F12 medium supplemented with 10% fetal bovine serum, tissue biopsies from upper turbinate have generated an adherent population of cells expressing mainly mesenchymal stromal phenotypic markers. A closer examination of these cells has also found co-expression of olfactory precursors and ensheathing cell phenotypic markers. These results were suggestive of a unique property of olfactory mesenchymal stromal cells as potentially olfactory progenitor cells.Objective: To study whether the expression of these proteins in mesenchymal stromal cells is modulated upon neuronal differentiation.Materials and methods: We observed the phenotype of olfactory stromal cells under DMEM/F12 plus 10% fetal bovine serum in comparison to cells from spheres induced by serum-free medium plus growth factors inducers of neural progenitors.Results: The expression of mesenchymal stromal (CD29+, CD73+, CD90+, CD45-), horizontal basal (ICAM-1/CD54+, p63+, p75NGFr+), and ensheathing progenitor cell (nestin+, GFAP+) proteins was determined in the cultured population by flow cytometry. The determination of Oct 3/4, Sox-2, and Mash-1 transcription factors, as well as the neurotrophins BDNF, NT3, and NT4 by RT-PCR in cells, was indicative of functional heterogeneity of the olfactory mucosa tissue sample. Conclusions: Mesenchymal and olfactory precursor proteins were downregulated by serum-free medium and promoted differentiation of mesenchymal stromal cells into neurons and astroglial cells.

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Perico, Norberto, Federica Casiraghi, and Giuseppe Remuzzi. "Clinical Translation of Mesenchymal Stromal Cell Therapies in Nephrology." Journal of the American Society of Nephrology 29, no. 2 (November 30, 2017): 362–75. http://dx.doi.org/10.1681/asn.2017070781.

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Mesenchymal stromal cells have emerged as potential candidates for cell-based therapies to modulate the immune response in organ transplantation and repair tissues after acute or chronic injury. Preclinical studies have shown convincingly in rodent models that mesenchymal stromal cells can prolong solid organ graft survival and that they can induce immune tolerance, accelerate recovery from AKI, and promote functional improvement in chronic nephropathies. Multiple complex properties of the cells, including immunomodulatory, anti-inflammatory, and proregenerative effects, seem to contribute. The promising preclinical studies have encouraged investigators to explore the safety, tolerability, and efficacy of mesenchymal stromal cell–based therapy in pilot clinical trials, including those for bone marrow and solid organ transplantation, autoimmune diseases, and tissue and organ repair. Here, we review the available data on culture-expanded mesenchymal stromal cells tested in renal transplantation, AKI, and CKD. We also briefly discuss the relevant issues that must be addressed to ensure rigorous assessment of the safety and efficacy of mesenchymal stromal cell therapies to allow the translation of this research into the practice of clinical nephrology.

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Genovese, Luca, and Andrea Brendolan. "Lymphoid Tissue Mesenchymal Stromal Cells in Development and Tissue Remodeling." Stem Cells International 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/8419104.

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Secondary lymphoid organs (SLOs) are sites that facilitate cell-cell interactions required for generating adaptive immune responses. Nonhematopoietic mesenchymal stromal cells have been shown to play a critical role in SLO function, organization, and tissue homeostasis. The stromal microenvironment undergoes profound remodeling to support immune responses. However, chronic inflammatory conditions can promote uncontrolled stromal cell activation and aberrant tissue remodeling including fibrosis, thus leading to tissue damage. Despite recent advancements, the origin and role of mesenchymal stromal cells involved in SLO development and remodeling remain unclear.

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Burnham, Andre J., Lisa P. Daley-Bauer, and Edwin M. Horwitz. "Mesenchymal stromal cells in hematopoietic cell transplantation." Blood Advances 4, no. 22 (November 24, 2020): 5877–87. http://dx.doi.org/10.1182/bloodadvances.2020002646.

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Abstract Mesenchymal stromal cells (MSCs) are widely recognized to possess potent immunomodulatory activity, as well as to stimulate repair and regeneration of diseased or damaged tissue. These fundamental properties suggest important applications in hematopoietic cell transplantation. Although the mechanisms of therapeutic activity in vivo are yet to be fully elucidated, MSCs seem to suppress lymphocytes by paracrine mechanisms, including secreted mediators and metabolic modulators. Most recently, host macrophage engulfment of apoptotic MSCs has emerged as an important contributor to the immune suppressive microenvironment. Although bone marrow–derived MSCs are the most commonly studied, the tissue source of MSCs may be a critical determinant of immunomodulatory function. The key application of MSC therapy in hematopoietic cell transplantation is to prevent or treat graft-versus-host disease (GVHD). The pathogenesis of GVHD reveals multiple potential targets. Moreover, the recently proposed concept of tissue tolerance suggests a new possible mechanism of MSC therapy for GVHD. Beyond GVHD, MSCs may facilitate hematopoietic stem cell engraftment, which could gain greater importance with increasing use of haploidentical transplantation. Despite many challenges and much doubt, commercial MSC products for pediatric steroid-refractory GVHD have been licensed in Japan, conditionally licensed in Canada and New Zealand, and have been recommended for approval by an FDA Advisory Committee in the United States. Here, we review key historical data in the context of the most salient recent findings to present the current state of MSCs as adjunct cell therapy in hematopoietic cell transplantation.

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Petrella, Francesco, Isabella Rimoldi, Stefania Rizzo, and Lorenzo Spaggiari. "Mesenchymal Stromal Cells for Antineoplastic Drug Loading and Delivery." Medicines 4, no. 4 (November 23, 2017): 87. http://dx.doi.org/10.3390/medicines4040087.

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Mesenchymal stromal cells are a population of undifferentiated multipotent adult cells possessing extensive self-renewal properties and the potential to differentiate into a variety of mesenchymal lineage cells. They express broad anti-inflammatory and immunomodulatory activity on the immune system and after transplantation can interact with the surrounding microenvironment, promoting tissue healing and regeneration. For this reason, mesenchymal stromal cells have been widely used in regenerative medicine, both in preclinical and clinical settings. Another clinical application of mesenchymal stromal cells is the targeted delivery of chemotherapeutic agents to neoplastic cells, maximizing the cytotoxic activity against cancer cells and minimizing collateral damage to non-neoplastic tissues. Mesenchymal stem cells are home to the stroma of several primary and metastatic neoplasms and hence can be used as vectors for targeted delivery of antineoplastic drugs to the tumour microenvironment, thereby reducing systemic toxicity and maximizing antitumour effects. Paclitaxel and gemcitabine are the chemotherapeutic drugs best loaded by mesenchymal stromal cells and delivered to neoplastic cells, whereas other agents, like pemetrexed, are not internalized by mesenchymal stromal cells and therefore are not suitable for advanced antineoplastic therapy. This review focuses on the state of the art of advanced antineoplastic cell therapy and its future perspectives, emphasizing in vitro and in vivo preclinical results and future clinical applications.

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Szala, Stanisław, Ewa Wiśniewska, and Justyna Czapla. "Mesenchymal Stromal Cells." Postępy Higieny i Medycyny Doświadczalnej 68 (November 13, 2014): 1287–98. http://dx.doi.org/10.5604/17322693.1128671.

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Bernardo, Maria Ester, Franco Locatelli, and Willem E. Fibbe. "Mesenchymal Stromal Cells." Annals of the New York Academy of Sciences 1176, no. 1 (September 2009): 101–17. http://dx.doi.org/10.1111/j.1749-6632.2009.04607.x.

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Lalu, Manoj M., Lauralyn L. McIntyre, and Duncan J. Stewart. "Mesenchymal stromal cells." Critical Care Medicine 40, no. 4 (April 2012): 1373–75. http://dx.doi.org/10.1097/ccm.0b013e31824317f7.

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Keating, Armand. "Mesenchymal stromal cells." Current Opinion in Hematology 13, no. 6 (November 2006): 419–25. http://dx.doi.org/10.1097/01.moh.0000245697.54887.6f.

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Horwitz, Edwin M., Michael Andreef, and Francesco Frassoni. "Mesenchymal Stromal Cells." Biology of Blood and Marrow Transplantation 13 (January 2007): 53–57. http://dx.doi.org/10.1016/j.bbmt.2006.10.016.

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Song, Haixin, Zi Yin, Tao Wu, Yangzheng Li, Xun Luo, Mingzhu Xu, Lihong Duan, and Jianhua Li. "Enhanced Effect of Tendon Stem/Progenitor Cells Combined With Tendon-Derived Decellularized Extracellular Matrix on Tendon Regeneration." Cell Transplantation 27, no. 11 (October 9, 2018): 1634–43. http://dx.doi.org/10.1177/0963689718805383.

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Decellularized extracellular matrices have been clinically used for tendon regeneration. However, only a few systematic studies have compared tendon stem/progenitor cells to mesenchymal stromal cells on the tendon-derived decellularized matrix. In the present study, we prepared extracellular matrix derived from porcine tendons and seeded with tendon stem/progenitor cells, embryonic stem cell-derived mesenchymal stromal cells or without stem cells. Then we implanted the mixture (composed of stem cells and scaffold) into the defect of a rat Achilles tendon. Next, 4 weeks post-surgery the regenerated tendon tissue was collected. Histological staining, immunohistochemistry, determination of collagen content, transmission electron microscopy, and biomechanical testing were performed to evaluate the tendon structure and biomechanical properties. Our study collectively demonstrated that decellularized extracellular matrix derived from porcine tendons significantly promoted the regeneration of injured tendons when combined with tendon stem/progenitor cells or embryonic stem cell-mesenchymal stromal cells. Compared to embryonic stem cell-mesenchymal stromal cells, tendon stem/progenitor cells combined with decellularized matrix showed more improvement in the structural and biomechanical properties of regenerated tendons in vivo. These findings suggest a promising strategy for functional tendon tissue regeneration and further studies are warranted to develop a functional tendon tissue regeneration utilizing tendon stem/progenitor cells integrated with a tendon-derived decellularized matrix.

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Zhu, H. B., D. Z. Guo, S. J. Yang, Y. H. Zhang, H. Wang, H. T. Guo, Y. Zhang, and D. C. Cheng. "Osteogenic actions of the osteogenic growth peptide on bovine marrow mesenchymal stromal cells in culture." Veterinární Medicína 53, No. 9 (October 16, 2008): 501–9. http://dx.doi.org/10.17221/1981-vetmed.

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The osteogenic growth peptide (OGP) regulates the differentiation of marrow mesenchymal stem cells derived from human and rodent cell lines into osteoblasts. Whether OGP directly regulates the bovine marrow mesenchymal stem cells differentiating into osteoblasts remains unknown. In this study, we evaluated the effects of OGP on the growth and differentiation of bovine marrow mesenchymal stem cells in culture. Our results showed that OGP promoted osteogenic differentiation of the bovine stem cells. OGP increased alkaline phosphatase (ALP) activity and mineralized nodule formation, and stimulated osteoblast-specific mRNA expression of Osteocalcin (BGP). On the other hand, OGP dose-dependently stimulated the expression of endothelial nitric oxide synthases. These results show for the first time a direct osteogenic effect of OGP on bovine marrow stromal cells in culture, which could be mediated by induction of endothelial nitric oxide synthases.

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Cammarota, Francesca, and Mikko O. Laukkanen. "Mesenchymal Stem/Stromal Cells in Stromal Evolution and Cancer Progression." Stem Cells International 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/4824573.

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The study of cancer biology has mainly focused on malignant epithelial cancer cells, although tumors also contain a stromal compartment, which is composed of stem cells, tumor-associated fibroblasts (TAFs), endothelial cells, immune cells, adipocytes, cytokines, and various types of macromolecules comprising the extracellular matrix (ECM). The tumor stroma develops gradually in response to the needs of epithelial cancer cells during malignant progression initiating from increased local vascular permeability and ending to remodeling of desmoplastic loosely vascularized stromal ECM. The constant bidirectional interaction of epithelial cancer cells with the surrounding microenvironment allows damaged stromal cell usage as a source of nutrients for cancer cells, maintains the stroma renewal thus resembling a wound that does not heal, and affects the characteristics of tumor mesenchymal stem/stromal cells (MSCs). Although MSCs have been shown to coordinate tumor cell growth, dormancy, migration, invasion, metastasis, and drug resistance, recently they have been successfully used in treatment of hematopoietic malignancies to enhance the effect of total body irradiation-hematopoietic stem cell transplantation therapy. Hence, targeting the stromal elements in combination with conventional chemotherapeutics and usage of MSCs to attenuate graft-versus-host disease may offer new strategies to overcome cancer treatment failure and relapse of the disease.

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Seyed-Razavi, Yashar, Brenda Williams, David A. Winkler, and Ivan Bertoncello. "Mesenchymal stromal cell turnover in the normal adult lung revisited." American Journal of Physiology-Lung Cellular and Molecular Physiology 305, no. 9 (November 1, 2013): L635—L641. http://dx.doi.org/10.1152/ajplung.00092.2013.

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We have employed a simple and robust noninvasive method of continuous in vivo long-term bromodeoxyuridine (BrdU) labeling to analyze lung mesenchymal stromal cell turnover in adult mice in the steady state. Mathematical modeling of BrdU uptake in flow cytometrically sorted CD45negCD31negSca-1poslung cells following long-term feeding of BrdU to mice in their drinking water reveals that lung mesenchymal stromal cells cycle continuously throughout life. Analysis of BrdU incorporation during long-term feeding and during chasing (delabeling) following replacement of BrdU-water with normal water shows that the CD45negCD31negSca-1poslung mesenchymal stromal cell compartment turns over at a rate of ∼2.26% per day with a time to half-cycled of 44 days, an estimated cell proliferation rate of 0.004/day, and a cell death rate of 0.018/day.

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Brouard, Nathalie, Camille Jost, Nadine Matthias, Camille Albrecht, Sébastien Egard, Poojabahen Gandhi, Catherine Strassel, et al. "A unique microenvironment in the developing liver supports the expansion of megakaryocyte progenitors." Blood Advances 1, no. 21 (September 26, 2017): 1854–66. http://dx.doi.org/10.1182/bloodadvances.2016003541.

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Key Points Two types of fetal liver stromal cell populations are identified: mesenchymal cells and prehepatic cells. The prehepatic stromal cell population exhibits a unique capacity to support the production of megakaryocytes from human and mouse HSCs.

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Payushina, Olga V. "Hematopoietic Microenvironment in the Fetal Liver: Roles of Different Cell Populations." ISRN Cell Biology 2012 (October 23, 2012): 1–7. http://dx.doi.org/10.5402/2012/979480.

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Hematopoiesis is the main function of the liver during a considerable period of mammalian prenatal development. Hematopoietic cells of the fetal liver exist in a specific microenvironment that controls their proliferation and differentiation. This microenvironment is created by different cell populations, including epitheliocytes, macrophages, various stromal elements (hepatic stellate cells, fibroblasts, myofibroblasts, vascular smooth muscle and endothelial cells, mesenchymal stromal cells), and also cells undergoing epithelial-to-mesenchymal transition. This paper considers the involvement of these cell types in the regulation of fetal liver hematopoiesis.

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Lina, Yani, and Andi Wijaya. "Adipose-Derived Stem Cells for Future Regenerative System Medicine." Indonesian Biomedical Journal 4, no. 2 (August 1, 2012): 59. http://dx.doi.org/10.18585/inabj.v4i2.164.

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BACKGROUND: The potential use of stem cell-based therapies for repair and regeneration of various tissues and organs offers a paradigm shift that may provide alternative therapeutic solutions for a number of disease. Despite the advances, the availability of stem cells remaining a challenge for both scientist and clinicians in pursuing regenerative medicine. CONTENT: Subcutaneous human adipose tissue is an abundant and accessible cell source for applications in tissue engineering and regenerative medicine. Routinely, the adipose issue is digested with collagenase or related lytic enzymes to release a heterogeneous population for stromal vascular fraction (SVF) cells. The SVF cells can be used directly or can be cultured in plastic ware for selection and expansion of an adherent population known as adipose-derived stromal/stem cells (ASCs). Their potential in the ability to differentiate into adipogenic, osteogenic, chondrogenic and other mesenchymal lineages, as well in their other clinically useful properties, includes stimulation of angiogenesis and suppression of inflammation.SUMMARY: Adipose tissue is now recognized as an accessible, abundant and reliable site for the isolation of adult stem cels suitable for the application of tissue engineering and regenerative medicine applications. The past decade has witnessed an explosion of preclinical data relating to the isolation, characterization, cryopreservation, differentiation, and transplantation of freshly isolated stromal vascular fraction cells and adherent, culture-expanded, adipose-derived stromal/stem cells in vitro and in animal models.KEYWORDS: adipose tissue, adult stem cells, regenerative medicine, mesenchymal stem cells

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Cilloni, Daniela, Carmelo Carlo-Stella, Franca Falzetti, Gabriella Sammarelli, Ester Regazzi, Simona Colla, Vittorio Rizzoli, Franco Aversa, Massimo F. Martelli, and Antonio Tabilio. "Limited engraftment capacity of bone marrow–derived mesenchymal cells following T-cell–depleted hematopoietic stem cell transplantation." Blood 96, no. 10 (November 15, 2000): 3637–43. http://dx.doi.org/10.1182/blood.v96.10.3637.h8003637_3637_3643.

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The engraftment capacity of bone marrow–derived mesenchymal cells was investigated in 41 patients who had received a sex-mismatched, T-cell–depleted allograft from human leukocyte antigen (HLA)–matched or –mismatched family donors. Polymerase chain reaction (PCR) analysis of the human androgen receptor (HUMARA) or the amelogenin genes was used to detect donor-derived mesenchymal cells. Only 14 marrow samples (34%) from 41 consenting patients generated a marrow stromal layer adequate for PCR analysis. Monocyte-macrophage contamination of marrow stromal layers was reduced below the levels of sensitivity of HUMARA and amelogenin assays (5% and 3%, respectively) by repeated trypsinizations and treatment with the leucyl-leucine (leu-leu) methyl ester. Patients who received allografts from 12 female donors were analyzed by means of the HUMARA assay, and in 5 of 12 cases a partial female origin of stromal cells was demonstrated. Two patients who received allografts from male donors were analyzed by amplifying the amelogenin gene, and in both cases a partial male origin of stromal cells was shown. Fluorescent in situ hybridization analysis using a Y probe confirmed the results of PCR analysis and demonstrated in 2 cases the existence of a mixed chimerism at the stromal cell level. There was no statistical difference detected between the dose of fibroblast progenitors (colony-forming unit–F [CFU-F]) infused to patients with donor- or host-derived stromal cells (1.18 ± 0.13 × 104/kg vs 1.19 ± 0.19 × 104/kg; P ≥ .97). In conclusion, marrow stromal progenitors reinfused in patients receiving a T-cell–depleted allograft have a limited capacity of reconstituting marrow mesenchymal cells.

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Wang, Chun Yan, Huo Tan, Zhen Qian Huang, Hai Ming Li, Dan Liu, and Run Hui Zheng. "Study on Effect Hemopoiesis Reconstituted of Auto-Mesenchymal Stromal Cells or Allo-Mesenchymal Stromal Cells Transplantion." Blood 110, no. 11 (November 16, 2007): 5056. http://dx.doi.org/10.1182/blood.v110.11.5056.5056.

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Abstract Objective: To study effect hemopoiesis reconstituted of auto-mesenchymal stromal cells (MSCs) or allo-mesenchymal stromal cells transplantion. Methods: MSCs were obtained from transplantion patient or embryo by culturing in Zhongshan university stem cell center. 2 patient(SLE, lymphoma) were transplant auto-MSCs before transplantion auto- haemopoietic stem cell(HSC), MSCs were 2.43×107/kg,2.76×107/kg, CD34+ cells were 2.13×104/kg,2.54×104/kg. 2 patient(CML, lymphoma) were transplant allo-MSCs(from embryo) after transplantion (+60 and +180), patient with CML was allo-HSCT, patient with lymphoma was auto-HSCT. MSCs were 2.23×105/kg. Rasults: 2 patients with combination transplantation auto-MSCs and auto-HSC were not adverse effect, neutrophil≥0.5 ×109/ L were +1 day and +10 day, platelet ≥20 ×109/ L were +1day and +8 day, granulocyte deficiency time were 0day and 7days. Two patients were complete remission(273 day and 124 day). Another two patient hemopoiesis delay (after transplantation +60 and +180) were transplanted allo-MSCs(from embryo), one patient with CML rised blood cell after transplantion, but 10 days later the patient relapsed, bone marrow showed acute transformation of chronic myelocytic leukemia. The patient died due to giving up trentment. The patient with lymphoma were transplanted allo-MSCs (from embryo), blood cells transient rised, but blood cells decreased after one week. Now the patient were complete remission (+300 day), but blood cells were lower. The two MSCs (from embryo) transplantation were failure. Conclusion: It is important that how to chose the MScs transplantation time. Combination transplantation auto-MSCs and auto-HSC can promote hemopoiesis re-establish, especially to fit old age patient. If patient with hemopoiesis delay after transplantation were trantplanted allo-MSCs maybe further research. [ key word] MSCs, transplantation, haemopoietic stem cell, hemopoiesis re-establish

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Abou Ezzi, Grazia, Teerawit Suparkorndej, Bryan Anthony, Jingzhu Zhang, Shilpi Ganguly, Roberto Civitelli, and Daniel C. Link. "Loss of TGF-β Signaling in Bone Marrow Mesenchymal Progenitors Promotes Adipocyte over Osteoblast Differentiation but Does Not Disrupt the HSC Niche." Blood 126, no. 23 (December 3, 2015): 666. http://dx.doi.org/10.1182/blood.v126.23.666.666.

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Abstract Hematopoietic stem cells (HSCs) reside in specialized microenvironments (niches) in the bone marrow. Several mesenchymal stromal cells have been implicated in hematopoietic niches, including osteoblasts, pericytes, CXCL12-abundant reticular (CAR) cells, and mesenchymal stem cells (MSCs). Members of the transforming growth factor (TGF) superfamily, in particular TGF-β, have a well-documented role in regulating osteoblast development. However, the contribution of TGF family member signaling to the establishment and maintenance of hematopoietic niches is largely unknown. Here, we characterize the role of transforming growth factor-β (TGF-β) signaling in mesenchymal stromal cells on the HSC niche. TGF-β receptor 2 (encoded by Tgfbr2) is required for all TGF-β signaling. To selectively disrupt TGF-β signaling in bone marrow mesenchymal stromal cells, we generated Osx-C re Tgfbr2fl/fl mice. Osx-Cre targets most bone marrow mesenchymal stromal cells (including osteoblasts, CAR cells, MSCs, pericytes, and adipocytes) but not endothelial cells or hematopoietic cells. Osx-C re Tgfbr2fl/fl mice are severely runted and most die by 4 weeks of age. We analyzed mice at 3 weeks, when the mice appeared healthy. Osteoblast number was severely reduced in Osx-C re Tgfbr2fl/fl mice, as assessed by histomorphometry and immunostaining for osteocalcin. Accordingly, microCT analysis demonstrated reduced tissue mineral density and cortical thickness of long bone and marked trabecularization of long bones in diaphyseal regions. Surprisingly, marrow adiposity, as measured by osmium tetroxide staining with microCT, was strikingly increased in Osx-C re Tgfbr2fl/fl mice. CAR cells are mesenchymal progenitors with osteogenic and adipogenic potential in vitro. To assess CAR cells, we generated Osx-Cre Tgfrb2fl/fl x Cxcl12gfp mice. Surprisingly, CAR cell number was significantly increased. However, despite the increase in CAR cells, the number of CFU-osteoblast (CFU-OB) in Osx-C re Tgfbr2fl/fl mice is nearly undetectable. Together, these data suggest that TGF-b signaling contributes to lineage commitment of mesenchymal progenitors. Specifically, our data suggest that TGF-β signaling suppresses commitment to the osteoblast lineage, while increasing adipogenic differentiation. We next asked whether alterations in bone marrow stromal cells present in Osx-C re Tgfbr2fl/fl mice affect HSC number or function. The increase in marrow adipocytes and loss of osteolineage cells is predicted to impair HSC maintenance, while the increase in CAR cells might augment HSCs. Osx-Cre Tgfrb2fl/fl mice have modest leukopenia, but normal red blood cell and platelet counts. Bone marrow and spleen cellularity are reduced, even after normalizing for body weight. The frequency of phenotypic HSCs (defined as Kit+ lineage- Sca+ CD34- Flk2- cells) is comparable to control mice. To assess HSC function, we performed competitive repopulation assays with bone marrow from Osx-Cre Tgfrb2fl/fl or control mice. Surprisingly, these data show that the long-term multi-lineage repopulating activity of HSCs from Osx-Cre Tgfrb2fl/fl mice is normal. Moreover, serial transplantation studies suggest that the self-renewal capacity of HSCs is normal. Thus, despite major alterations in mesenchymal stromal cell populations, the HSC niche is intact in Osx-Cre Tgfrb2fl/fl mice. Collectively, these data show that TGF-b signaling in mesenchymal progenitors is required for the proper development of multiple stromal cell populations that contribute to hematopoietic niches. Studies are underway to assess the impact of post-natal deletion of Tgfbr2 in mesenchymal stromal cell on hematopoietic niches. Since drugs that modulate the activity of TGF-b are in development, this research may suggest novel approaches to modulate hematopoietic niches for therapeutic benefit. Disclosures No relevant conflicts of interest to declare.

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Kim, Christopher, and Armand Keating. "Cell Therapy for Knee Osteoarthritis: Mesenchymal Stromal Cells." Gerontology 65, no. 3 (2019): 294–98. http://dx.doi.org/10.1159/000496605.

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Hematti, Peiman. "Human embryonic stem cell-derived mesenchymal stromal cells." Transfusion 51 (November 2011): 138S—144S. http://dx.doi.org/10.1111/j.1537-2995.2011.03376.x.

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Bernardo, Maria Ester, and Willem E. Fibbe. "Mesenchymal stromal cells and hematopoietic stem cell transplantation." Immunology Letters 168, no. 2 (December 2015): 215–21. http://dx.doi.org/10.1016/j.imlet.2015.06.013.

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Kucerova, Lucia, Miroslava Matuskova, Kristina Hlubinova, Veronika Altanerova, and Cestmir Altaner. "Tumor cell behaviour modulation by mesenchymal stromal cells." Molecular Cancer 9, no. 1 (2010): 129. http://dx.doi.org/10.1186/1476-4598-9-129.

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Lupatov, Alexey Yu, Roza Yu Saryglar, Valentina V. Vtorushina, Rimma A. Poltavtseva, Oxana A. Bystrykh, Vladimir D. Chuprynin, Lyubov V. Krechetova, Stanislav V. Pavlovich, Konstantin N. Yarygin, and Gennady T. Sukhikh. "Mesenchymal Stromal Cells Isolated from Ectopic but Not Eutopic Endometrium Display Pronounced Immunomodulatory Activity In Vitro." Biomedicines 9, no. 10 (September 22, 2021): 1286. http://dx.doi.org/10.3390/biomedicines9101286.

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A comparative analysis of the cell surface markers and immunological properties of cell cultures originating from normal endometrium and endometrioid heterotopias of women with extragenital endometriosis was carried out. Both types of cell cultures expressed surface molecules typical of mesenchymal stromal cells and did not express hematopoietic and epithelial markers. Despite similar phenotype, the mesenchymal stromal cells derived from the two sources had different immunomodulation capacities: the cells of endometrioid heterotopias but not eutopic endometrium could suppress dendritic cell differentiation from monocytes as well as lymphocyte proliferation in allogeneic co-cultures. A comparative multiplex analysis of the secretomes revealed a significant increase in the secretion of pro-inflammatory mediators, including IL6, IFN-γ, and several chemokines associated with inflammation by the stromal cells of ectopic lesions. The results demonstrate that the stromal cells of endometrioid heterotopias display enhanced pro-inflammatory and immunosuppressive activities, which most likely impact the pathogenesis and progression of the disease.

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Muraglia, A., R. Cancedda, and R. Quarto. "Clonal mesenchymal progenitors from human bone marrow differentiate in vitro according to a hierarchical model." Journal of Cell Science 113, no. 7 (April 1, 2000): 1161–66. http://dx.doi.org/10.1242/jcs.113.7.1161.

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Bone marrow stromal cells can give rise to several mesenchymal lineages. The existence of a common stem/progenitor cell, the mesenchymal stem cell, has been proposed, but which developmental stages follow this mesenchymal multipotent progenitor is not known. Based on experimental evidence, a model of mesenchymal stem cell differentiation has been proposed in which individual lineages branch directly from the same progenitor. We have verified this model by using clonal cultures of bone marrow derived stromal fibroblasts. We have analyzed the ability of 185 non-immortalized human bone marrow stromal cell clones to differentiate into the three main lineages: osteo-, chondro- and adipogenic. All clones but one differentiated into the osteogenic lineage. About one third of the clones differentiated into all three lineages analyzed. Most clones (60-80%) displayed an osteo-chondrogenic potential. We have never observed clones with a differentiation potential limited to the osteo-adipo- or to the chondro-adipogenic phenotype, nor pure chondrogenic and adipogenic clones. How long the differentiation potential of a number of clones was maintained was assessed throughout their life span. Clones progressively lost their adipogenic and chondrogenic differentiation potential at increasing cell doublings. Our data suggest a possible model of predetermined bone marrow stromal cells differentiation where the tripotent cells can be considered as early mesenchymal progenitors that display a sequential loss of lineage potentials, generating osteochondrogenic progenitors which, in turn, give rise to osteogenic precursors.

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Koch, Matthias, Felix P. Achatz, Siegmund Lang, Christian G. Pfeifer, Girish Pattappa, Richard Kujat, Michael Nerlich, Peter Angele, and Johannes Zellner. "Tissue Engineering of Large Full-Size Meniscus Defects by a Polyurethane Scaffold: Accelerated Regeneration by Mesenchymal Stromal Cells." Stem Cells International 2018 (May 7, 2018): 1–11. http://dx.doi.org/10.1155/2018/8207071.

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The endogenous healing potential of avascular meniscal lesions is poor. Up to now, partial meniscectomy is still the treatment of choice for meniscal lesions within the avascular area. However, the large loss of meniscus substance predisposes the knee for osteoarthritic changes. Tissue engineering techniques for the replacement of such lesions could be a promising alternative treatment option. Thus, a polyurethane scaffold, which is already in clinical use, loaded with mesenchymal stromal cells, was analyzed for the repair of critical meniscus defects in the avascular zone. Large, approximately 7 mm broad meniscus lesions affecting both the avascular and vascular area of the lateral rabbit meniscus were treated with polyurethane scaffolds either loaded or unloaded with mesenchymal stromal cells. Menisci were harvested at 6 and 12 weeks after initial surgery. Both cell-free and cell-loaded approaches led to well-integrated and stable meniscus-like repair tissue. However, an accelerated healing was achieved by the application of mesenchymal stromal cells. Dense vascularization was detected throughout the repair tissue of both treatment groups. Overall, the polyurethane scaffold seems to promote the vessel ingrowth. The application of mesenchymal stromal cells has the potential to speed up the healing process.

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Cilloni, Daniela, Carmelo Carlo-Stella, Franca Falzetti, Gabriella Sammarelli, Ester Regazzi, Simona Colla, Vittorio Rizzoli, Franco Aversa, Massimo F. Martelli, and Antonio Tabilio. "Limited engraftment capacity of bone marrow–derived mesenchymal cells following T-cell–depleted hematopoietic stem cell transplantation." Blood 96, no. 10 (November 15, 2000): 3637–43. http://dx.doi.org/10.1182/blood.v96.10.3637.

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Abstract The engraftment capacity of bone marrow–derived mesenchymal cells was investigated in 41 patients who had received a sex-mismatched, T-cell–depleted allograft from human leukocyte antigen (HLA)–matched or –mismatched family donors. Polymerase chain reaction (PCR) analysis of the human androgen receptor (HUMARA) or the amelogenin genes was used to detect donor-derived mesenchymal cells. Only 14 marrow samples (34%) from 41 consenting patients generated a marrow stromal layer adequate for PCR analysis. Monocyte-macrophage contamination of marrow stromal layers was reduced below the levels of sensitivity of HUMARA and amelogenin assays (5% and 3%, respectively) by repeated trypsinizations and treatment with the leucyl-leucine (leu-leu) methyl ester. Patients who received allografts from 12 female donors were analyzed by means of the HUMARA assay, and in 5 of 12 cases a partial female origin of stromal cells was demonstrated. Two patients who received allografts from male donors were analyzed by amplifying the amelogenin gene, and in both cases a partial male origin of stromal cells was shown. Fluorescent in situ hybridization analysis using a Y probe confirmed the results of PCR analysis and demonstrated in 2 cases the existence of a mixed chimerism at the stromal cell level. There was no statistical difference detected between the dose of fibroblast progenitors (colony-forming unit–F [CFU-F]) infused to patients with donor- or host-derived stromal cells (1.18 ± 0.13 × 104/kg vs 1.19 ± 0.19 × 104/kg; P ≥ .97). In conclusion, marrow stromal progenitors reinfused in patients receiving a T-cell–depleted allograft have a limited capacity of reconstituting marrow mesenchymal cells.

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Coccè, Valentina, Anna Brini, Aldo Bruno Giannì, Valeria Sordi, Angiola Berenzi, Giulio Alessandri, Carlo Tremolada, Silvia Versari, Antonio Bosetto, and Augusto Pessina. "A Nonenzymatic and Automated Closed-Cycle Process for the Isolation of Mesenchymal Stromal Cells in Drug Delivery Applications." Stem Cells International 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/4098140.

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The adipose tissue is a good source of mesenchymal stromal cells that requires minimally invasive isolation procedures. To ensure reproducibility, efficacy, and safety for clinical uses, these procedures have to be in compliant with good manufacturing practices. Techniques for harvesting and processing human adipose tissue have rapidly evolved in the last years, and Lipogems® represents an innovative approach to obtain microfragmented adipose tissue in a short time, without expansion and/or enzymatic treatment. The aim of this study was to assess the presence of mesenchymal stromal cells in the drain bag of the device by using a prototype Lipogems processor to wash the lipoaspirate in standardized condition. We found that, besides oil and blood residues, the drain bag contained single isolated cells easy to expand and with the typical characteristics of mesenchymal stromal cells that can be loaded with paclitaxel to use for drug-delivery application. Our findings suggest the possibility to replace the drain bag with a “cell culture chamber” obtaining a new integrated device that, without enzymatic treatment, can isolate and expand mesenchymal stromal cells in one step with high good manufacturing practices compliance. This system could be used to obtain mesenchymal stromal cells for regenerative purposes and for drug delivery.

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FENYO, IOANA MADALINA, ANA-MARIA VACARU, ANCA VIOLETA GAFENCU, and MIHAI BOGDAN PREDA. "A method for in vivo tracking of mesenchymal stromal cells after intrapancreatic delivery." Romanian Biotechnological Letters 26, no. 3 (April 11, 2021): 2707–13. http://dx.doi.org/10.25083/rbl/26.3/2707-2713.

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Background and aim. The intrapancreatic injection of mesenchymal stromal cells may be a viable delivery route for experimental therapy in type 1 diabetes. Adequate in vivo cell imaging is important to evaluate the treatment efficiency, the fate of the transplanted cells, and the mechanisms of the effects observed. Here, we present a technique for delivering these cells into the mouse pancreas and tracking them using fluorescent near-infrared quantum dots and in vivo imaging. Methods and results. Bone marrow-derived mesenchymal stromal cells isolated from NOD mice were cultured and labeled with Qdots 800 nanocrystals, before being injected in the pancreas of pre-diabetic mice. In vivo analysis (IVIS Spectrum system) showed that the cells were successfully injected and remained localized in the pancreas for at least 24 hours. Conclusions. Labeling of mesenchymal stromal cells with Qdots 800 nanocrystals is a reliable method for in vivo cell tracking, after local delivery in the pancreas.

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Hochheuser, Caroline, Nina Y. Kunze, Godelieve A. M. Tytgat, Carlijn Voermans, and Ilse Timmerman. "The Potential of Mesenchymal Stromal Cells in Neuroblastoma Therapy for Delivery of Anti-Cancer Agents and Hematopoietic Recovery." Journal of Personalized Medicine 11, no. 3 (February 25, 2021): 161. http://dx.doi.org/10.3390/jpm11030161.

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Neuroblastoma is one of the most common pediatric cancers and a major cause of cancer-related death in infancy. Conventional therapies including high-dose chemotherapy, stem cell transplantation, and immunotherapy approach a limit in the treatment of high-risk neuroblastoma and prevention of relapse. In the last two decades, research unraveled a potential use of mesenchymal stromal cells in tumor therapy, as tumor-selective delivery vehicles for therapeutic compounds and oncolytic viruses and by means of supporting hematopoietic stem cell transplantation. Based on pre-clinical and clinical advances in neuroblastoma and other malignancies, we assess both the strong potential and the associated risks of using mesenchymal stromal cells in the therapy for neuroblastoma. Furthermore, we examine feasibility and safety aspects and discuss future directions for harnessing the advantageous properties of mesenchymal stromal cells for the advancement of therapy success.

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Abomaray, Fawaz, Sebastian Gidlöf, Bartosz Bezubik, Mikael Engman, and Cecilia Götherström. "Mesenchymal Stromal Cells Support Endometriotic Stromal CellsIn Vitro." Stem Cells International 2018 (2018): 1–12. http://dx.doi.org/10.1155/2018/7318513.

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Endometriosis is an inflammatory disease marked by ectopic growth of endometrial cells. Mesenchymal stromal cells (MSC) have immunosuppressive properties that have been suggested as a treatment for inflammatory diseases. Therefore, the aim herein was to examine effects of allogeneic MSC on endometriosis-derived cellsin vitroas a potential therapy for endometriosis. MSC from allogeneic adipose tissue (Ad-MSC) and stromal cells from endometrium (ESCendo) and endometriotic ovarian cysts (ESCcyst) from women with endometriosis were isolated. The effects of Ad-MSC on ESCendoand ESCcystwere investigated usingin vitroproliferation, apoptosis, adhesion, tube formation, migration, and invasion assays. Ad-MSC significantly increased proliferation of ESC compared to untreated controls. Moreover, Ad-MSC significantly decreased apoptosis and increased survival of ESC. Ad-MSC significantly increased adhesion of ESCendoand not ESCcyston fibronectin. Conditioned medium from cocultures of Ad-MSC and ESC significantly increased tube formation of human umbilical vein endothelial cells on matrigel. Ad-MSC may significantly increase migration of ESCcystand did not increase invasion of both cell types. The data suggest that allogeneic Ad-MSC should not be considered as a potential therapy for endometriosis, because they may support the pathology by maintaining and increasing growth of ectopic endometrial tissue.

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Estève, David, Jean Galitzky, Anne Bouloumié, Caroline Fonta, René Buchet, and David Magne. "Multiple Functions of MSCA-1/TNAP in Adult Mesenchymal Progenitor/Stromal Cells." Stem Cells International 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/1815982.

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Our knowledge about mesenchymal stem cells has considerably grown in the last years. Since the proof of concept of the existence of such cells in the 70s by Friedenstein et al., a growing mass of reports were conducted for a better definition of these cells and for the reevaluation from the term “mesenchymal stem cells” to the term “mesenchymal stromal cells (MSCs).” Being more than a semantic shift, concepts behind this new terminology reveal the complexity and the heterogeneity of the cells grouped in MSC family especially as these cells are present in nearly all adult tissues. Recently, mesenchymal stromal cell antigen-1 (MSCA-1)/tissue nonspecific alkaline phosphatase (TNAP) was described as a new cell surface marker of MSCs from different tissues. The alkaline phosphatase activity of this protein could be involved in wide range of MSC features described below from cell differentiation to immunomodulatory properties, as well as occurrence of pathologies. The present review aims to decipher and summarize the role of TNAP in progenitor cells from different tissues focusing preferentially on brain, bone marrow, and adipose tissue.

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Chateauvieux, Sebastien, Jean-Laurent Ichanté, Bruno Delorme, Vincent Frouin, Geneviève Piétu, Alain Langonné, Nathalie Gallay, et al. "Molecular profile of mouse stromal mesenchymal stem cells." Physiological Genomics 29, no. 2 (April 2007): 128–38. http://dx.doi.org/10.1152/physiolgenomics.00197.2006.

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We determined a transcriptional profile specific for clonal stromal mesenchymal stem cells from adult and fetal hematopoietic sites. To identify mesenchymal stem cell-like stromal cell lines, we evaluated the adipocytic, osteoblastic, chondrocytic, and vascular smooth muscle differentiation potential and also the hematopoietic supportive (stromal) capacity of six mouse stromal cell lines from adult bone marrow and day 14.5 fetal liver. We found that two lines were quadripotent and also supported hematopoiesis, BMC9 from bone marrow and AFT024 from fetal liver. We then ascertained the set of genes differentially expressed in the intersection set of AFT024 and BMC9 compared with those expressed in the union set of two negative control lines, 2018 and BFC012 (both from fetal liver); 346 genes were upregulated and 299 downregulated. Using Ingenuity software, we found two major gene networks with highly significant scores. One network contained downregulated genes that are known to be implicated in osteoblastic differentiation, proliferation, or transformation. The other network contained upregulated genes that belonged to two categories, cytoskeletal genes and genes implicated in the transcriptional machinery. The data extend the concept of stromal mesenchymal stem cells to clonal cell populations derived not only from bone marrow but also from fetal liver. The gene networks described should discriminate this cell type from other types of stem cells and help define the stem cell state.

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Plava, Jana, Marina Cihova, Monika Burikova, Martin Bohac, Marian Adamkov, Slavka Drahosova, Dominika Rusnakova, et al. "Permanent Pro-Tumorigenic Shift in Adipose Tissue-Derived Mesenchymal Stromal Cells Induced by Breast Malignancy." Cells 9, no. 2 (February 19, 2020): 480. http://dx.doi.org/10.3390/cells9020480.

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During cancer progression, breast tumor cells interact with adjacent adipose tissue, which has been shown to be engaged in cancer aggressiveness. However, the tumor-directed changes in adipose tissue-resident stromal cells affected by the tumor–stroma communication are still poorly understood. The acquired changes might remain in the tissue even after tumor removal and may contribute to tumor relapse. We investigated functional properties (migratory capacity, expression and secretion profile) of mesenchymal stromal cells isolated from healthy (n = 9) and tumor-distant breast adipose tissue (n = 32). Cancer patient-derived mesenchymal stromal cells (MSCs) (MSC-CA) exhibited a significantly disarranged secretion profile and proliferation potential. Co-culture with MDA-MB-231, T47D and JIMT-1, representing different subtypes of breast cancer, was used to analyze the effect of MSCs on proliferation, invasion and tumorigenicity. The MSC-CA enhanced tumorigenicity and altered xenograft composition in immunodeficient mice. Histological analysis revealed collective cell invasion with a specific invasive front of EMT-positive tumor cells as well as invasion of cancer cells to the nerve-surrounding space. This study identifies that adipose tissue-derived mesenchymal stromal cells are primed and permanently altered by tumor presence in breast tissue and have the potential to increase tumor cell invasive ability through the activation of epithelial-to-mesenchymal transition in tumor cells.

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de Jong, Madelon M. E., Zoltan Kellermayer, Natalie Papazian, M. Duin, Annemiek Broyl, Pieter Sonneveld, and Tom Cupedo. "Single Cell Transcriptomic Analysis of the Multiple Myeloma Bone Marrow Identifies a Unique Inflammatory Stromal Cell Population Associated with TNF Signaling." Blood 134, Supplement_1 (November 13, 2019): 690. http://dx.doi.org/10.1182/blood-2019-123012.

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Background: In multiple myeloma, tumor cell survival, disease progression and therapy response are influenced by signals derived from the non-malignant bone marrow niche. This notwithstanding, a detailed in-vivo definition of the cells that define the multiple myeloma niche is lacking. Mesenchymal stromal cells are important niche constituents. Recent progress made with single cell transciptomics suggests that mesenchymal stromal cells are a dynamic population of cells that can exist as several subsets with functionally distinct activation and differentiation profiles. Aim: To identify mesenchymal stromal cell subsets specific for the multiple myeloma bone marrow niche, by comparing stromal cells from myeloma patients to non-cancer controls. Methods: The non-hematopoietic bone marrow niche was isolated from viably frozen bone marrow aspirates from 10 newly diagnosed multiple myeloma patients (6 hyperdiploid, 3 t(11;14) and 1 with deletion of 17p) and 2 non-cancer controls using high speed cell sorting. The purified cells were analyzed by 10X Genomics single cell sequencing directly post-thawing, without prior cell culture. From 10 multiple myeloma patients we generated single cell transcriptomes with an average read-depth of 20,000 reads per cell of in total 12,000 niche cells and from the 2 non-cancer controls a total of 3,500 niche cells. Transcriptomes were pooled and subjected to clustering analyses using the Seurat package for R to identify genetically distinct clusters of niche cells and changes in these clusters associated specifically with multiple myeloma. Results: The bioinformatical analyses generated 10 distinct clusters of niche cells, all of which were present in both non-cancer and multiple myeloma bone marrow. One of these clusters contained CDH5+ endothelial cells while the remaining 9 clusters were subsets of CXCL12+LEPR+ mesenchymal stromal cells. Because samples were taken from the central marrow by aspiration, peripheral endosteal or neuronal lineage cells were not represented in these clusters. Gene Set Enrichment Analysis (GSEA) of the stromal cell clusters from myeloma versus non-cancer controls revealed two significantly altered pathways: TNF signaling via NF-kB and Inflammatory response. Detailed analyses of the individual stromal cell clusters identified two clusters that were responsible for the inflammatory changes identified by GSEA. Both clusters were present in all myeloma patients, constituted on average 20% of total stromal cells and were defined by transcription of the inflammatory chemokines CXCL2, CXCL3 and CXCL8 the cytokine IL6. All these transcripts were absent from the equivalent clusters in control bone marrow. The presence of inflammatory stroma in the multiple myeloma niche indicates either the appearance of a novel stromal cell subset, or activation of pre-existing stromal cells. GSEA analyses suggested inflammatory signaling, and to functionally confirm this, we tested whether activation of stromal cells would induce the inflammatory stromal phenotype. Stimulation of primary human stromal cells in vitro with recombinant TNF was sufficient to induce transcription of CXCL2, CXCL3 and CXCL8, recapitulating the inflammatory transcriptome. Moreover, manual removal of these TNF target genes from the in-silico clustering analyses led to a merging of the inflammatory clusters with non-inflammatory clusters. This indicates that the major distinguishing feature of the myeloma-specific stromal cells are genes induced upon stromal cell activation. Conclusion: Through single cell transcriptomic analyses we have identified the presence of activated inflammatory stromal cells associated with TNF signaling in the multiple myeloma stromal niche. These inflammatory stromal cells are reminiscent of pathogenic cancer-associated fibroblasts found in solid tumors, where these cells create a pro-tumorigenic niche that favors tumor survival and proliferation while simultaneously inhibiting anti-cancer immunity. These findings represent the first description of myeloma-specific stromal cell subsets, and provide novel cellular targets for interventions aimed at disrupting the pro-tumorigenic microenvironment in multiple myeloma. Disclosures Broyl: Celgene, amgen, Janssen,Takeda: Honoraria. Sonneveld:Amgen: Honoraria, Research Funding; BMS: Honoraria; Celgene: Honoraria, Research Funding; Janssen: Honoraria, Research Funding; SkylineDx: Research Funding; Takeda: Honoraria, Research Funding; Karyopharm: Honoraria, Research Funding.

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Volkova, N. А. "MULTIPOTENT MESENCHYMAL STROMAL CELLS OF BONE MARROW IN THERAPY OF CHRONIC INFLAMMATION OF THE MURINE OVARIES." Biotechnologia acta 7, no. 5 (2014): 35–42. http://dx.doi.org/10.15407/biotech7.05.035.

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Zou, Ji-Ping, Sha Huang, Yan Peng, Hong-Wei Liu, Biao Cheng, Xiao-Bing Fu, and Xiao-Fei Xiang. "Mesenchymal Stem Cells/Multipotent Mesenchymal Stromal Cells (MSCs)." International Journal of Lower Extremity Wounds 11, no. 4 (October 30, 2012): 244–53. http://dx.doi.org/10.1177/1534734612463935.

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Ghilzon, R., C. A. G. McCulloch, and R. Zohar. "Stromal Mesenchymal Progenitor Cells." Leukemia & Lymphoma 32, no. 3-4 (January 1999): 211–21. http://dx.doi.org/10.3109/10428199909167382.

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Tolar, Jakub, and Miroslav Tolar. "Reinventing mesenchymal stromal cells." Cytotherapy 14, no. 4 (April 2012): 388–90. http://dx.doi.org/10.3109/14653249.2012.665631.

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Ghanta, Sailaja, Min-Young Kwon, Ivan O. Rosas, Xiaoli Liu, and Mark A. Perrella. "Mesenchymal Stromal Cell Therapy." Critical Care Medicine 46, no. 2 (February 2018): 343–45. http://dx.doi.org/10.1097/ccm.0000000000002894.

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Renzi, Sabrina, Tina Lombardo, Silvia Dotti, Sara S. Dessì, Pasquale De Blasio, and Maura Ferrari. "Mesenchymal Stromal Cell Cryopreservation." Biopreservation and Biobanking 10, no. 3 (June 2012): 276–81. http://dx.doi.org/10.1089/bio.2012.0005.

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Journal articles on the topic 'Mesenchynol stronel cels'

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