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Journal articles on the topic "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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Dissertations / Theses on the topic "Mesenchynol stronel cels"

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Caminal, Bobet Marta. "Tissue engineering for bone regeneration: in vitro development and in vivo testing in sheep." Doctoral thesis, Universitat Autònoma de Barcelona, 2014. http://hdl.handle.net/10803/285622.

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L'os és un teixit connectiu altament organitzat i especialitzat, la funció principal és la mecànica, proporcionant l'afecció als músculs i per tant permetent que el cos es mogui. Actualment, el tractament quirúrgic estàndard es basa en la immobilització i la introducció d'empelts ossis però presenta algunes complicacions, com ara les infeccions, les no unions i la morbiditat de la zona donant. Avui en dia, milions de pacients pateixen defectes ossis i en concret, als EEUU es diagnostiquen entre 10.000 i 20.000 nous casos d'osteonecrosi del cap de fèmur (ONFH) a l’any. La medicina regenerativa (RM) i l'enginyeria tissular (TE) són dos camps de la ciència que es centren en el desenvolupament de teràpies per reemplaçar i regenerar els teixits perduts o danyats per millorar la qualitat de vida del pacient. La combinació de biomaterials, cèl·lules i senyals és l’eina clau per al desenvolupament d'un producte RM i TE. Un dels camps més desenvolupats en RM és la medicina regenerativa ortopèdica, en concret per al teixit ossi. Hi ha diferents estratègies que combinen cèl·lules autòlogues amb matrius que han demostrat certa eficàcia en el tractament de lesions òssies. Després de la fase de descobriment de nous medicaments de teràpia avançada, i per tal d’aconseguir el registre del nou producte, hi ha la fase de desenvolupament, que inclou la realització d'estudis preclínics (fet per dur a terme la prova de concepte, la seguretat i toxicologia) i els estudis clínics. En primer lloc es van determinar i caracteritzar els components de la preparació d’enginyeria tissular (TEP) amb la finalitat d’obtenir un producte estandarditzat. Aquesta preparació consisteix en un component cel·lular que són les cèl·lules mesenquimals estromals (MSC), tant humanes com ovines unides en una matriu de partícules òssies desantigeneïtzades i liofilitzades. Es va realizar un model de defecte ossi de mida crítica (CSBD) en ovella amb la finalitat d'investigar l'efecte de la TEP en una situació extrema, i es va demostrar la seva seguretat i capacitat per sintetitzar nou os i remodelar l’os existent. Seguidament la TEP es va provar en un model animal rellevant de translació de la malaltia òssia basat en el mètode reportat per Vélez i col·laboradors per a la modelització de ONFH en ovelles demostrant la seva eficàcia i seguretat. També s’ha demostrat que les MSC estan involucrades en la síntesi d'os nou ja que es van trobar progenitors ossis marcats després del tractament de la ONFH, tot i així no es poden descartar els mecanismes paracrins. Per tant, el desenvolupament de la TEP podria contribuir en general a la RM per tal de satisfer les exigències d'una societat que envelleix.
Bone is a highly organized and specialized connective tissue, whose main function is the mechanics, providing attachment to muscles and therefore allowing the body to move. Currently the gold standard surgical treatment is based on the immobilization and introduction of bone grafts but it presents some complications, such as infections, non-unions, and donor site morbidity. Nowadays, millions of patients are suffering from bone defects and specifically, 10,000 to 20,000 new cases of osteonecrosis of femoral head (ONFH) are diagnosed only in the USA every year. Regenerative medicine (RM) and tissue engineering (TE) are two areas of science fields focused on the developing of therapies to replace and regenerate lost or damaged tissues to improve the quality of life the patient. The combination of biomaterials, cells and signals is the key tool for the development of a RM and TE product. One of the most developed fields in RM is the orthopedic regenerative medicine, in specifically for bone tissue. There are different strategies combining autologous cells with scaffolds that have shown some efficacy for treating bone injuries. After discovery phase of any new advanced therapy medicinal products, there is the development phase that includes the conduction of preclinical studies (made to perform the proof of concept, safety and toxicology) and clinical studies before the registration of the new product. First the components of the tissue engineered preparation (TEP) were determined and characterized in order to have a standardized material. It consists in MSC (mesenchymal stromal cells) both human and ovine sources are used as a cellular component seeded in a deantigenized and lyophilized bone particles as a scaffold. Then critical size bone defect (CSBD) was modeled in sheep in order to investigate the effect of the TEP in an extreme situation, demonstrating its safe ability to synthesize new bone and bone remodeling. Afterwards TEP was tested in a relevant translational animal model of bone disease based on the method reported by Velez and collaborators for modelling ONFH in sheep demonstrating its efficacy and safety. Also demonstrating that MSC were involved in the synthesis of new bone, because labeled bone progenitors are shown after ONFH treatment, although paracrine mechanisms can not be discarded. Therefore, the development of TEP could contribute to the overall RM to meet the requirements of an aging society.
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Nie, Yingjie. "Defective dendritic cells and mesenchymal stromal cells in systemic lupus erythematosus and the potential of mesenchymal stromal cells as cell-therapy." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43278681.

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Campos, Ana Margarida Ferreira. "Lipidomic analysis of mesenchymal cells candidates for cell therapy." Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/15275.

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Mestrado em Bioquímica - Métodos Biomoleculares
Mesenchymal stromal cells are adult stem cells found mostly in the bone marrow. They have immunosuppressive properties and they have been successfully applied as biological therapy in several clinical trials regarding autoimmune diseases. Despite the great number of clinical trials, MSCs’ action is not fully understand and there are no identified markers that correlate themselves with the immunomodulatory power. A lipidomic approach can solve some of these problems once lipids are one of the major cells’ components. Therefore, in this study cells’ lipidome was analysed and its deviations were evaluated according to the medium of culture and to the presence of pro-inflammatory stimuli, mimicking physiological conditions in which these cells are used. This was the first study ever made that aimed to analyse the differences in the phospholipid profile between mesenchymal stromal cells non-stimulated and stimulated with proinflammatory stimulus. This analysis was conducted in both cells cultured in medium supplemented with animal serum and in cells cultured in a synthetic medium. In cells cultured in the standard medium the levels of phosphatidylcholine (PC) species with shorter fatty acids (FAs) acyl chains decreased under pro-inflammatory stimuli. The level of PC(40:6) also decreased, which may be correlated with enhanced levels of lysoPC (LPC)(18:0) - an anti-inflammatory LPC - observed in cells subjected to TNF-α and IFN-γ. Simultaneously, the relative amounts of PC(36:1) and PC(38:4) increased. TNF-α and IFN- γ also enhanced the levels of phosphatidylethanolamine PE(40:6) and decreased the levels of PE(38:6). Higher expression of phosphatidylserine PS(36:1) and sphingomyelin SM(34:0) along with a decrease in PS(38:6) levels were observed. However, in cells cultured in a synthetic medium, TNF-α and IFN-γ only enhanced the levels of PS(36:1). These results indicate that lipid metabolism and signaling is modulated during mesenchymal stromal cells action.
As células mesenquimais do estroma são células estaminais adultas que apresentam propriedades imunossupressoras e têm sido aplicadas como terapia clínica em vários estudos clínicos relativos a doenças autoimunes. Apesar do vasto número de estudos clínicos que utilizam estas células, ainda não se conhece o mecanismo de ação das mesmas, nem foram ainda identificados marcadores permitam avaliar o seu potencial imunomodulador. A lipidómica poderá dar algumas respostas a estas questões uma vez que os lípidos são importantes componentes das células, desempenhando um papel na sinalização celular. No presente trabalho estudou-se o lipidoma das células mesenquimais e avaliou-se a sua variação consoante o meio de cultura e a presença de estímulos próinflamatórios, mimetizando as condições fisiológicas em que as células são utilizadas. Este foi o primeiro estudo que analisou as diferenças no perfil fosfolípidico entre células mesenquimais do estroma e avaliou a variação do lipidoma destas células após a sua estimulação por mediadores pró-inflamatórios. Este estudo foi conduzido num primeiro conjunto de células cultivado num meio padrão suplementado com soro animal e num segundo conjunto de células cultivado num meio sintético. Nas células cultivadas no meio padrão, observou-se uma diminuição nas espécies moleculares de fosfatidilcolina (PC) com cadeias de ácidos gordos (FAs) após estímulos pro-inflamatórios. A quantidade de PC(40:6) também diminuiu, relacionando-se com o aumento expressão de lisoPC (LPC)(18:0) – LPC anti-inflamatória – em células estimuladas. Simultaneamente, a quantidade relativa de PC(36:1) e PC(38:4) aumentou. TNF-α and IFN-γ também levou ao aumento dos níveis de fosfatidiletanolamina PE(40:6) e diminuiu os níveis de PE(38:6). Também se verificou um aumento da expressão de fosfatidilserina PS(36:1) e esfingomielina (SM)(34:0), bem como a diminuição na expressão de PS(38:6). Contudo, em células mesenquimais cultivadas em meio sintético, com TNF-α and IFN-γ apenas aumentaram os níveis de PS(36:1). Estes resultados indicam que o metabolismo dos lípidos é modulado durante a ação imunossupressora das células.
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Nie, Yingjie, and 聶瑛潔. "Defective dendritic cells and mesenchymal stromal cells in systemic lupus erythematosus and the potential of mesenchymal stromal cells ascell-therapy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43278681.

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Fung, Kwong-lam, and 馮廣林. "Chemoresistance induced by mesenchymal stromal cells on cancer cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/205639.

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Human mesenchymal stromal cells (hMSCs) are part of bone marrow micro-environment that supports hematopoiesis. However, hMSCs also enhance tumor progression and survival when they become part of the cancer micro-environment. I aimed to investigate the interaction between hMSCs and cancer cells during chemotherapy. Firstly, I studied the interaction between hMSCs and T-lineage acute lymphoblastic leukemia (T-ALL) cells under pegylated arginase I (BCT-100) treatment. Three T-ALL cell lines were sensitive to BCT-100 but not hMSCs. Conversely, hMSCs could partly protect all T-ALL cell lines from BCT-100 induced cell death under transwell co-culture condition. Concerning the possible mechanism, the intermediate metabolite L-ornithine could not rescue most T-ALL cells from BCT-100 treatment. But the downstream L-arginine precursor, L-citrulline could partly rescue all T-ALL cells from BCT-100 treatment. Ornithine transcarbamylase (OTC) converts L-ornithine into L-citrulline. OTC expression level in hMSCs remained relatively high during BCT-100 treatment but OTC expressions in T-ALL cell lines declined drastically. It suggested that hMSCs may protect T-ALL cells against BCT-100 treatment by having sustained OTC expression. Suppression of hMSCs by vincristine (VCR) disrupted the protective effect of hMSCs to most T-ALL cells during BCT-100 treatment. This suggests that by transiently suppressing hMSCs, we may abolish the protective effect of hMSCs to T-ALL cells during BCT-100 treatment. Then I studied the interaction between hMSCs and neuroblastoma under cisplatin treatment. Two neuroblastoma cell lines were used for both of them are cisplatin sensitive while hMSCs are cisplatin resistant. hMSCs could partly protect neuroblastoma cells from cisplatin induced cytotoxicity. On the other hand, exogenous IL-6 but not IL-8 could also partly rescue them from cisplatin induced cytotoxicity. IL-6 activated STAT3 phosphorylation dose-dependently and enhanced expression of detoxifying enzyme (glutathione S-transferase π, GST-π) in neuroblastoma. Such effect could be counteracted by anti-IL-6R neutralizing antibody tocilizumab (TCZ). However, TCZ failed to suppress hMSCs’ protection to neuroblastoma during cisplatin treatment. This suggests involvement of multiple factors. Up-regulation of serum GST-πin some hTertMSCs/neuroblastoma co-engrafted SCID mice compared to neuroblastoma engrafted mice provided a clue that GST-π might be a possible stromal-protection factor. Caffeic acid phenethyl ester (CAPE) is a known GST inhibitor after tyrosinase activation. Neuroblastoma cells expressed tyrosinase and CAPE enhanced cisplatin cytotoxicity on them, with or without hMSCs. Paradoxically, CAPE enhanced GST-πexpression with or without cisplatin treatment in neuroblastoma suggesting possible negative feedback to GST-π inhibition. However, such additive effect of CAPE to cisplatin cytotoxicity was not observed in vivo. Further delineation of the in vivo study design may help to verify the additive effect of CAPE to cisplatin cytotoxicity in vivo. Finally, I studied the effect of apoptotic cancer cells (AC) on the immune function of hMSCs. hMSCs could phagocytose apoptotic neuroblastoma cells with respective up-regulation of many immune-mediators including two highly-expressed cytokines IL-6 and IL-8. Up-regulation of these immune-mediators may enhance immune cells chemotaxis. Further detailed investigation on the effect of AC-engulfed hMSCs to other immune cells will help us to understand the dynamic interaction between cancer cells and stromal cells during chemotherapy.
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Paediatrics and Adolescent Medicine
Doctoral
Doctor of Philosophy
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Kühl, Tobias Hans-Jürgen [Verfasser], and Leena [Akademischer Betreuer] Bruckner-Tuderman. "Mesenchymal stromal cell therapy for dystrophic epidermolysis bullosa." Freiburg : Universität, 2016. http://d-nb.info/1119452716/34.

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Sory, David Roger Raymond. "Dynamic loading of periosteum-derived mesenchymal stromal cells." Thesis, Imperial College London, 2017. http://hdl.handle.net/10044/1/59138.

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Explosive-generated waves exhibit high-energy loading profiles featured with mechanical characteristics applied over a wide range of strain rates. Recent decades have seen unprecedented occurrence of high-energy trauma associated with blast wave exposure. One such blast-specific pathology is blast-induced heterotopic ossification (bHO), which refers to ectopic bone formation due to inappropriate mesenchymal stromal cell (MSC) osteogenesis in non-skeletal tissues. Significant effort has been made into deciphering the molecular mechanisms that allow the onset of bHO, however little research has been reported on the exact role of the biomechanical processes involved in transducing blast-associated mechanical stimuli into molecular events stimulating osteogenesis in MSCs. The research presented in this thesis investigated the stimulation of osteogenesis in periosteum-derived mesenchymal stromal cells (PO MSCs) in response to mechanical insults simulating blast landmine trauma. This involved the development of experimental biocompatible in vitro platforms and the tailoring of biomechanically-relevant stimuli of varying stress intensities (up to 70 MPa), and strain rates (0.01 to 3000 /s). Subsequently, cell health and the stimulation of osteogenesis were investigated by studying the expression of Runx2 and Osteocalcin (OC) genes. We found that cell health was not affected by single-pulse loadings of wide range of impulse levels (0.20 to 95000 N.s). We showed evidence of mechanically-stimulated osteogenesis in PO MSCs through the upregulation of Runx2 and OC genes in loaded samples. Furthermore, our results highlighted that the stimulation of osteogenesis in MSCs did not result solely from the effect a single mechanical parameter, but rather the combined action of several features. We showed that osteogenesis stimulation in MSCs arised from the complex interplay between the mechanical characteristics of the loading along with the environment used to convey the stress wave. Finally, our research indicated that PO MSCs are finely tuned to respond to mechanical stimuli that fall within defined parameters.
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Ward, Lewis Stuart Corey. "Interactions of mesenchymal stromal cells with their microenvironment." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8278/.

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Mesenchymal stromal cells (MSC) suppress the inflammatory infiltrate through crosstalk with neighbouring endothelium. However, this response is lost at chronic inflammatory sites where stromal cells instead support leukocyte recruitment and upregulate expression of podoplanin. The mechanism and function by which this inflammatory phenotype is established is unknown. We hypothesise that MSC modulation of endothelium is also altered by exposure to inflammatory cytokines, and that expression of podoplanin confers an invasive phenotype, enabling the interaction of these perivascular MSC with circulating platelets. MSC resisted functional transformation during acute or prolonged exposure to tumour necrosis factor alpha, instead maintaining their ability to suppress neutrophil recruitment in a flow-based assay. Expression of podoplanin promoted MSC migration through Ras-related C3 botulinum toxin substrate dependent signalling, enabling perivascular MSC to interact with cells confined to the circulation. Indeed, podoplanin induced the activation of platelets from flow through MSC protrusions in the endothelial lining. The retention of MSC suppressive function under inflammatory conditions supports their use in equivalent environments for therapy. However, the implications of platelet CLEC-2 activation by its ligand, podoplanin on inflamed stroma have yet to be elucidated and warrant further investigation, with specific focus drawn to the pathophysiology of thromboinflammation and associated disorders.
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Martella, Elisa <1984&gt. "Mesenchymal stromal cell: new applications for regenerative medicine." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5440/.

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In the last decades mesenchymal stromal cells (MSC), intriguing for their multilineage plasticity and their proliferation activity in vitro, have been intensively studied for innovative therapeutic applications. In the first project, a new method to expand in vitro adipose derived-MSC (ASC) while maintaining their progenitor properties have been investigated. ASC are cultured in the same flask for 28 days in order to allow cell-extracellular matrix and cell-cell interactions and to mimic in vivo niche. ASC cultured with this method (Unpass cells) were compared with ASC cultured under classic condition (Pass cells). Unpass and Pass cells were characterized in terms of clonogenicity, proliferation, stemness gene expression, differentiation in vitro and in vivo and results obtained showed that Unpass cells preserve their stemness and phenotypic properties suggesting a fundamental role of the niche in the maintenance of ASC progenitor features. Our data suggests alternative culture conditions for the expansion of ASC ex vivo which could increase the performance of ASC in regenerative applications. In vivo MSC tracking is essential in order to assess their homing and migration. Super-paramagnetic iron oxide nanoparticles (SPION) have been used to track MSC in vivo due to their biocompatibility and traceability by MRI. In the second project a new generation of magnetic nanoparticles (MNP) used to label MSC were tested. These MNP have been functionalized with hyperbranched poly(epsilon-lysine)dendrons (G3CB) in order to interact with membrane glycocalix of the cells avoiding their internalization and preventing any cytotoxic effects. In literature it is reported that labeling of MSC with SPION takes long time of incubation. In our experiments after 15min of incubation with G3CB-MNP more then 80% of MSC were labeled. The data obtained from cytotoxic, proliferation and differentiation assay showed that labeling does not affect MSC properties suggesting a potential application of G3CB nano-particles in regenerative medicine.
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Davies, Benjamin Michael. "Optimising mesenchymal stromal cell harvesting in orthopaedic surgery." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:aeb65824-d07b-4c73-bb51-aedaf7a7b0c2.

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Musculoskeletal tissue is prone to age-related degeneration and to damage which heals poorly. Many current treatments are able to treat only the end stages of these conditions, such as the use of total knee replacements in osteoarthritis. Cellular therapies are seen as a potential source of effective treatments for the earlier stages of these conditions. Orthopaedic surgery has been at the forefront of cellular therapies with treatments such as microfracture and autologous chondrocyte implantation to treat chondral defects. As the largest area of current cell therapy research, stem cells have become an area of high interest for developing novel treatments. Mesenchymal stromal cells (MSCs) have provided the basis of the majority of orthopaedic treatments because of the relative ease of obtaining them. Despite the development of a number of treatments using both freshly harvested MSCs and culture expanded MSCs there is still a large gap in our knowledge of the mechanisms of actions of these cells and the most appropriate locations for obtaining autologous samples. This thesis seeks to examine the best source of MSCs for surgery around the knee, comparing the pelvis to the femur and tibia. It also seeks to determine if it is possible to improve the yield of MSCs using a simple modification of the standard method of aspiration. Assessments of the yield of all cells and MSCs showed that the pelvis was the optimum source for MSCs in terms of cell numbers. There was also a large amount of inter-subject variation in the number of cells obtained. There was no difference in the functional abilities of cells from any location. Modification of the aspiration technique did not improve the cell yield. Future work should focus on improving yields from the pelvis and investigate methods of overcoming the inter-subject variability in yields if standardised treatments are to be successfully developed.
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Books on the topic "Mesenchynol stronel cels"

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Hematti, Peiman, and Armand Keating, eds. Mesenchymal Stromal Cells. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-5711-4.

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Gross, Gerhard, and Thomas Häupl. Stem cell-dependent therapies: Mesenchymal stem cells in chronic inflammatory disorders. Berlin: De Gruyter, 2013.

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Zhao, Robert Chunhua. Essentials of mesenchymal stem cell biology and its clinical translation. Dordrecht: Springer, 2013.

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Mesenchymal Stromal Cells. Elsevier, 2017. http://dx.doi.org/10.1016/c2014-0-03703-3.

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Mesenchymal Stromal Cells as Tumor Stromal Modulators. Elsevier, 2017. http://dx.doi.org/10.1016/c2014-0-03622-2.

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Mesenchymal Stromal Cells Biology And Clinical Applications. Springer-Verlag New York Inc., 2013.

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J, Prockop Darwin, Phinney Donald G, and Bunnell Bruce A, eds. Mesenchymal stem cells: Methods and protocols. Totowa, NJ: Humana Press, 2008.

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Keating, Armand, and Peiman Hematti. Mesenchymal Stromal Cells: Biology and Clinical Applications. Humana Press, 2013.

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Keating, Armand, and Peiman Hematti. Mesenchymal Stromal Cells: Biology and Clinical Applications. Humana, 2016.

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Stem Cell Therapeutics for Cancer. Wiley-Blackwell, 2013.

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Book chapters on the topic "Mesenchynol stronel cels"

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Bernardo, Maria Ester, and Franco Locatelli. "Mesenchymal Stromal Cells in Hematopoietic Stem Cell Transplantation." In Mesenchymal Stem Cells, 3–20. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3584-0_1.

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Shen, Yi, Poornima Venkat, Michael Chopp, and Jieli Chen. "Mesenchymal Stromal Cell Therapy of Stroke." In Cellular and Molecular Approaches to Regeneration and Repair, 217–37. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-66679-2_11.

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Gee, Adrian P. "MSCs: The US Regulatory Perspective." In Mesenchymal Stromal Cells, 343–54. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5711-4_17.

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Pittenger, Mark F. "Characterization of MSCs: From Early Studies to the Present." In Mesenchymal Stromal Cells, 59–77. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5711-4_4.

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Caplan, Arnold I. "MSCs as Therapeutics." In Mesenchymal Stromal Cells, 79–90. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5711-4_5.

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Hematti, Peiman, and Armand Keating. "Mesenchymal Stromal Cells in Regenerative Medicine: A Perspective." In Mesenchymal Stromal Cells, 3–16. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5711-4_1.

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Lozito, Thomas P., and Rocky S. Tuan. "Cross-Talk Between MSCs and Their Environments." In Mesenchymal Stromal Cells, 169–92. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5711-4_10.

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Wuchter, Patrick, and Anthony D. Ho. "Human MSCs from Bone Marrow, Umbilical Cord Blood, and Adipose Tissue: All the Same?" In Mesenchymal Stromal Cells, 193–208. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5711-4_11.

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Jacamo, Rodrigo, Erika Spaeth, Venkata Battula, Frank Marini, and Michael Andreeff. "MSCs in Solid Tumors and Hematological Malignancies: From Basic Biology to Therapeutic Applications." In Mesenchymal Stromal Cells, 209–35. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5711-4_12.

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Bunnell, Bruce A., Christine Gagliardi, and Maria Isabel Ribeiro Dias. "MSC Studies in Large-Animal Models." In Mesenchymal Stromal Cells, 237–58. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5711-4_13.

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Conference papers on the topic "Mesenchynol stronel cels"

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Van Dyke, William S., Ozan Akkus, and Eric Nauman. "Murine Osteochondral Stem Cells Express Collagen Type I More Strongly on PDMS Substrates Than on Tissue Culture Plastic." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14272.

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The discovery of the multipotent lineage of mesenchymal stem cells has dawned a new age in tissue engineering, where an autologous cell-seeded scaffold can be implanted into different therapeutic sites. Mesenchymal stem cells have been reported to differentiate into numerous anchorage-dependent cell phenotypes, including neurons, adipocytes, myoblasts, chondrocytes, tenocytes, and osteoblasts. A seminal work detailing that mesenchymal stem cells can be directed towards differentiation of different cell types by substrate stiffness alone [1] has led to numerous studies attempting to understand how cells can sense the stiffness of their substrate [2–3] Substrate stiffness has been shown to be an inducer of stem cell differentiation. MSCs on extremely soft substrates (250 Pa), similar to the stiffness of bone marrow, became quiescent but still retained their multipotency [4]. Elastic substrates in the stiffness range of 34 kPa revealed MSCs with osteoblast morphology, and osteocalcin along with other osteoblast markers were expressed [1]. However, osteogenesis has been found to increase on much stiffer (20–80 kPa) [5–6] (400 kPa) [7] as well as much softer substrates (75 Pa) [8]. Overall, cells have increased projected cell area and proliferation on stiffer substrates, leading to higher stress fiber formation. This study seeks to understand if the stiffness of the substrate has any effect on the differentiation potential of osteochondral progenitor cells into bone cells, using an in vitro dual fluorescent mouse model.
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Lalu, Manoj M., Lauralyn McIntyre, Christina Pugliese, and Duncan J. Stewart. "Safety Of Cell Therapy With Mesenchymal Stromal Cells (MSCs): A Systematic Review." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6043.

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Campbell, Jared M., Abbas Habibalahi, Saabah B. Mahbub, Sharon Paton, Stan Gronthos, and Ewa M. Goldys. "Multispectral characterisation of mesenchymal stem/stromal cells: age, cell cycle, senescence, and pluripotency." In Label-free Biomedical Imaging and Sensing (LBIS) 2020, edited by Natan T. Shaked and Oliver Hayden. SPIE, 2020. http://dx.doi.org/10.1117/12.2544623.

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Coughlin, Thomas R., Matthew Haugh, Muriel Voisin, Evelyn Birmingham, Laoise M. McNamara, and Glen L. Niebur. "Primary Cilia Knockdown Reduces the Number of Stromal Cells in Three Dimensional Ex Vivo Culture." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14723.

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Mesenchymal stem cells (MSCs) are multipotent stromal cells that reside in the bone marrow and differentiate into connective cell lines, such as adipocytes and osteoblasts [1]. An appropriate balance of MSC differentiation toward adipocytes and osteoblasts is vital to bone homeostasis [6]. In vitro work demonstrates that differentiation of MSCs is influenced by mechanical stimuli [2, 3]. In a mouse model, the ratio of adipocytes to MSCs in the marrow was 19% lower compared to controls following treatment by low magnitude mechanical signals (LMMS) [4]. In mice, LMMS increased MSC number by 46% and the differentiation capacity of MSCs was biased towards osteoblastic compared to adipogenic differentiation [5]. Thus, mechanobiological stimuli may play an important role in maintaining balanced MSC differentiation.
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Piñeiro-Ramil, María, Rocío Castro-Viñuelas, Clara Sanjurjo-Rodríguez, Silvia Rodríguez-Fernández, Tamara Hermida Gómez, Francisco Javier de-Toro-Santos, Francisco J. Blanco, Isaac Fuentes-Boquete, and Silvia Maria Díaz-Prado. "AB0102 GENERATION OF OSTEOARTHRITIC MESENCHYMAL STROMAL CELL LINES." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.6717.

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Kihira, Kentaro, Hiroki Hori, Shotaro Iwamoto, and Yoshihiro Komada. "Abstract 458: B cell precursor ALL cells alter their immunophenotype, cell cycle, and chemosensitivity through contact with mesenchymal stromal cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-458.

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Weaver, Aaron S., Yu-Ping Su, Dana L. Begun, Ralph T. Zade, Andrea I. Alford, Kurt D. Hankenson, Jaclynn M. Kreider, Stephanie A. Ablowitz, Michael R. Kilbourn, and Steven A. Goldstein. "Systemic Mesenchymal Stem Cell Delivery and Axial Mechanical Stimulation Accelerate Fracture Healing." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192554.

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Fracture healing is a complex process involving numerous cell types, whose actions are regulated by many factors in their local environment. Mechanical factors are known to exert a strong influence on the actions of these cells and the progression of the repair process. While prior studies have investigated the effect of physical forces on cell differentiation, biofactor expression, and mechanical competence of repair, the mechanosensory and response mechanisms are poorly understood. This study was designed to explore the influence of a controlled mechanical environment on temporal aspects of the bone repair process. Specifically, this study examines how the timing of an applied strain influences local cell behavior during fracture repair, and how this load affects the migration of systemically introduced mesenchymal stem cells (MSCs) to the fracture site.
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Nakata, Rie, Lucia Borriello, Muller Fabbri, Hiroyuki Shimada, and Yves A. Declerck. "Abstract 5076: Tumor cell-derived exosomes educate bone marrow mesenchymal stromal cells toward a protumorigenic function." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5076.

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Brady, Jack, Shahd Horie, Claire Masterson, Declan Byrnes, Hector Gonzalez, Daniel O'Toole, and John Laffey. "Mesenchymal Stromal Cells Modulate the Systemic and Pulmonary Immune Cell Profile in Klebsiella Pneumoniae Induced Sepsis." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1060.

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Popp, Henning D., Vanessa Kohl, Alice Fabarius, Oliver Drews, Miriam Bierbaum, Ahmed Jawhar, Ali Darwich, et al. "Genotoxic bystander signals from irradiated human mesenchymal stromal cells mainly localize in the 10 – 100 kDa fraction of conditioned medium." In Cell-to-Cell Metabolic Cross-Talk in Physiology and Pathology. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/cells2020-08925.

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