共查询到20条相似文献,搜索用时 15 毫秒
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Lazennec G 《Médecine sciences : M/S》2011,27(3):285-288
Mesenchymal stem cells (MSC) have attracted recent attention for their cell therapy potential, based in particular on their immunosuppressive properties, which have served as the basis for the treatment of autoimmune diseases. Interestingly, MSC have been used in cell therapy strategies to deliver therapeutical genes. Cell therapy approaches taking advantages of MSC have been proposed, as MSC display a potential tropsim for tumors. However, all these strategies raise a series of questions about the safety of MSC, as MSC could enhance tumor growth and metastasis. This review summarizes recent findngs about MSC in carcinogenesis. 相似文献
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David M. Poitz Friedrich Stölzel Laleh Arabanian Jens Friedrichs Denitsa Docheva Matthias Schieker Fernando A. Fierro Uwe Platzbecker Rainer Ordemann Carsten Werner Martin Bornhäuser Ruth H. Strasser Gerhard Ehninger Thomas Illmer 《Biochimica et Biophysica Acta (BBA)/Molecular Cell Research》2013,1833(12):3396-3404
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Feng Xu Yue Hu Jiebai Zhou Xiangdong Wang 《Journal of cellular and molecular medicine》2013,17(8):927-935
Acute lung injury (ALI) is a severe clinical condition responsible for high mortality and the development of multiple organ dysfunctions, because of the lack of specific and effective therapies for ALI. Increasing evidence from pre‐clinical studies supports preventive and therapeutic effects of mesenchymal stem cells (MSCs, also called mesenchymal stromal cells) in ALI/ARDS (acute respiratory distress syndrome). Therapeutic effects of MSCs were noticed in various delivery approaches (systemic, local, or other locations), multiple origins (bone marrow or other tissues), or different schedules of administrations (before or after the challenges). MSCs could reduce the over‐production of inflammatory mediators, leucocyte infiltration, tissue injury and pulmonary failure, and produce a number of benefit factors through interaction with other cells in the process of lung tissue repair. Thus, it is necessary to establish guidelines, standard operating procedures and evaluation criteria for translating MSC‐based therapies into clinical application for patients with ALI. 相似文献
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Intervention with mesenchymal stem cells (MSCs) represents a promising therapeutic tool in treatment-refractory autoimmune
diseases. A new report by Schurgers and colleagues in a previous issue of Arthritis Research & Therapy sheds novel mechanistic insight into the pathways employed by MSCs to suppress T-cell proliferation in vitro, but, at the same time, indicates that MSCs do not influence T-cell reactivity and the disease course in an in vivo arthritis model. Such discrepancies between the in vitro and in vivo effects of potent cellular immune modulators should spark further research and should be interpreted as a sign of caution
for the in vitro design of MSC-derived interventions in the setting of human autoimmune diseases. 相似文献
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Kakkar Anupama Nandy Sushmita Bose Gupta Suchi Bharagava Balram Airan Balram Mohanty Sujata 《Molecular and cellular biochemistry》2019,450(1-2):53-64
Molecular and Cellular Biochemistry - S100A11 as a S100 protein family member has been documented to play dual-direction regulation over cancer cell proliferation. We explored the role of S100A11... 相似文献
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Dario Siniscalco James Jeffrey Bradstreet Nataliia Sych Nicola Antonucci 《World journal of stem cells》2014,6(2):173-178
Autism spectrum disorders(ASDs)are complex neurodevelopmental disorders characterized by dysfunctions in social interactions,abnormal to absent verbal communication,restricted interests,and repetitive stereotypic verbal and non-verbal behaviors,influencing the ability to relate to and communicate.The core symptoms of ASDs concern the cognitive,emotional,and neurobehavioural domains.The prevalence of autism appears to be increasing at an alarming rate,yet there is a lack of effective and definitive pharmacological options.This has created an increased sense of urgency,and the need to identify novel therapies.Given the growing awareness of immune dysregulation in a significant portion of the autistic population,cell therapies have been proposed and applied to ASDs.In particular,mesenchymal stem cells(MSCs)possess the immunological properties which make them promising candidates in regenerative medicine.MSC therapy may be applicable to several diseases associated with inflammation and tissue damage,where subsequent regeneration and repair is necessary.MSCs could exert a positive effect in ASDs through the following mechanisms:stimulation of repair in the damaged tissue,e.g.,inflammatory bowel disease;synthesizing and releasing anti-inflammatory cytokines and survival-promoting growth factors;integrating into existing neural and synaptic network,and restoring plasticity.The paracrine mechanisms of MSCs show interesting potential in ASD treatment.Promising and impressive results have been reported from the few clinical studies published to date,although the exact mechanisms of action of MSCs in ASDs to restore functions are still largely unknown.The potential role of MSCs in mediating ASD recovery is discussed in light of the newest findings from recent clinical studies. 相似文献
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Bhandari DR Seo KW Sun B Seo MS Kim HS Seo YJ Marcin J Forraz N Roy HL Larry D Colin M Kang KS 《Differentiation; research in biological diversity》2011,82(3):144-152
Diabetes mellitus is a challenging autoimmune disease. Biomedical researchers are currently exploring efficient and effective ways to solve this challenge. The potential of stem cell therapies for treating diabetes represents one of the major focuses of current research on diabetes treatment. Here, we have attempted to differentiate adult stem cells from umbilical cord blood-derived mesenchymal cells (UCB-MSC), Wharton's jelly-derived mesenchymal stem cells (WJ-MSC) and amniotic epithelial stem cells (AE-SC) into insulin-producing cells. The serum-free protocol developed in this study resulted in the differentiation of cells into definitive endoderm, pancreatic foregut, pancreatic endoderm and, finally, pancreatic endocrine cells, which expressed the marker genes SOX17, PDX1, NGN3, NKX6.1, INS, GCG, and PPY, respectively. Detection of the expression of the gap junction-related gene connexin-36 (CX36) using RT-PCR provided conclusive evidence for insulin-producing cell differentiation. In addition to this RT-PCR result, insulin and C-peptide protein were detected by immunohistochemistry and ELISA. Glucose stimulation test results showed that significantly greater amounts of C-peptide and insulin were released from differentiated cells than from undifferentiated cells. In conclusion, the methods investigated in this study can be considered an effective and efficient means of obtaining insulin-producing cells from adult stem cells within a week. 相似文献
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Si-Dong Yang Lei Ma Ti-Xin Gu Wen-Yuan Ding Feng Zhang Yong Shen Ying-Ze Zhang Da-Long Yang Di Zhang Ya-Peng Sun Yan-Li Song 《Apoptosis : an international journal on programmed cell death》2014,19(5):789-800
Levofloxacin has been reported to have cytotoxicity to chondrocytes in vitro. And 17β-estradiol has been widely studied for its protective effects against cell apoptosis. Based on apoptotic cell model induced by levofloxacin, the purpose of this study was to explore the mechanism by which 17β-estradiol protects rat nucleus pulposus cells from apoptosis. Inverted phase-contrast microscopy, flow cytometry, and caspase-3 activity assay were used to find that levofloxacin induced marked apoptosis, which was abolished by 17β-estradiol. Interestingly, estrogen receptor antagonist, ICI182780, and functional blocking antibody to α2β1 integrin, both prohibited the effect of 17β-estradiol. Simultaneously, levofloxacin decreased cellular binding ability to type II collagen, which was also reversed by 17β-estradiol. Furthermore, western blot and real-time quantitative PCR were used to find that integrin α2β1 was responsible for estrogen-dependent anti-apoptosis, which was time–response and dose–response effect. 17β-estradiol was proved for the first time to protect rat nucleus pulposus cells against levofloxacin-induced apoptosis by upregulating integrin α2β1 signal pathway. 相似文献
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Uccelli A Morando S Bonanno S Bonanni I Leonardi A Mancardi G 《Current stem cell research & therapy》2011,6(1):69-72
The lack of therapies fostering remyelination and regeneration of the neural network deranged by the autoimmune attack occurring in multiple sclerosis (MS), is raising great expectations about stem cells therapies for tissue repair. Mesenchymal stem cells (MSCs) have been proposed as a possible treatment for MS due to the reported capacity of transdifferentiation into neural cells and their ability at modulating immune responses. However, recent studies have demonstrated that many other functional properties are likely to play a role in the therapeutic plasticity of MSCs, including anti-apoptotic, trophic and anti-oxidant effects. These features are mostly based on the paracrine release of soluble molecules, often dictated by local environmental cues. Based on the modest evidence of long-term engraftment and the striking clinical effects that are observed immediately after MSCs administration in the experimental model of MS, we do not favor a major role for transdifferentiation as an important mechanism involved in the therapeutic effect of MSCs. 相似文献
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Summary Platelet-derived growth factor (PDGF) and transforming growth factor beta-1(TGF-β1) were tested separately or together for
the ability to stimulate migration of human aortic vascular smooth muscle cells (VSMC). PDGF (10 ng/ml) stimulated migration
of VSMC over a 48-h period. TGF-β1 (10 ng/ml) had no effect on migration during the same period. VSMC exposed simultaneously
to both TGF-β1 and PDGF exhibited diminished migration (50%) when compared to cells treated only with PDGF. Cells that migrated
in the presence of PDGF possessed short actin cables that extended from cellular processes at the leading edge of migrating
cells; focal adhesions containing the αvβ3/β5 integrins localized to the same region. Cells grown in the presence of TGF-β1 exhibited long, intensely stained actin filaments
that spanned the entire length of the cell and were similar to untreated control VSMC. Focal adhesions containing αvβ3/β5 distributed evenly on the basal surface in both TGF-β1-treated cells and control cultures. Cellular responses to PDGF were
mitigated when TGF-β1 was present in the culture medium. VSMC grown in the presence of both PDGF and TGF-β1 exhibited elongated
actin filaments that were similar to nonmotile TGF-β1-treated cultures. Concomitant exposure of VSMC to PDGF and TGF-β1 resulted
in focal adhesions that distributed evenly on the lower cell surface. This study suggests that TGF-β1 can partially reverse
the stimulatory effect of PDGF on VSMC migration in vitro by modifying the actin cytoskeleton and the distribution of the α
vβ3/β5 integrins. 相似文献
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Parkinson’s disease (PD) is an age-related neurodegenerative disease caused by the progressive loss of dopaminergic (DA) neurons in the substantia nigra. As DA neurons degenerate, PD patients gradually lose their ability of movement. To date no effective therapies are available for the treatment of PD and its pathogenesis remains unknown. Experimental models that appropriately mimic the development of PD are certainly needed for gaining mechanistic insights into PD pathogenesis and identifying new therapeutic targets. Human induced pluripotent stem cells (iPSCs) could provide a promising model for fundamental research and drug screening. In this review, we summarize various iPSCs-based PD models either derived from PD patients through reprogramming technology or established by gene-editing technology, and the promising application of iPSC-based PD models for mechanistic studies and drug testing. 相似文献
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Tingting Xu Nuoya Liu Ying Shao Yujie Huang Danyan Zhu 《Journal of cellular biochemistry》2019,120(3):4355-4365
MicroRNAs (miRNAs) have been identified as key players in cardiogenesis and heart pathophysiological processes. However, many miRNAs are still not recognized for their roles in cardiomyocytes differentiation. In this study, we evaluated the effects of microRNA-218 (miR-218) in cardiomyocyte differentiation of the mouse embryonic stem cells (ESCs) in vitro. The percentage of the beating embryoid bodies (EBs) in miR-218 mimic-treated cells was reduced to 32% compared with miR-218 mimic negative control (56%) on day 5 + 3. The amplitude of the intracellular Ca2+ transients in the cardiomyocytes derived from ESCs was reduced upon miR-218 overexpression, followed by the decreased calcium-related proteins and cell junction proteins expressions. Besides, miR-218 expression in ESCs was related to the directional spreading ability of EBs during differentiation. The increased expression of miR-218 could promote the migration of ESCs in vitro, while the decreased expression of miR-218 could inhibit the migration by the transwell experiment. Meanwhile, miR-218 could regulate cell migration–related proteins Cdc42 and Rac1. Platelet-derived growth factor receptor α (PDGFRα) was further confirmed to be a direct target of miR-218 both physically and functionally by dual-luciferase reporter assay. Our data further described that overexpression of PDGFRα rescued the miR-218-mediated inhibition of cardiomyocyte differentiation and restored the miR-218-mediated promotion of cell migration. In conclusion, miR-218 was demonstrated to exert an inhibitory function and promoted cell migration via targeting PDGFRα during cardiomyocyte differentiation from ESCs. The current study revealed the role of miR-218 and may provide an important hint for cardiomyocyte differentiation of ESCs and induced pluripotent stem cells. 相似文献
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Hu CC Ke YQ Sun XL Jiang XD Xu RX Lv J Wang YS Cai YQ Qin LS Zou YX 《Biotechnology letters》2009,31(2):181-189
Human mesenchymal stem cells-like cells (hMSCs-like cells) were used as a tumor treatment platform for the systemic delivery
of immunotoxin genes. VEGF165-PE38 recombinant immunotoxin served as the model system. hMSCs-like cells were isolated, expanded,
and electroporated with the pIRES2-VEGF165PE38-EGFP plasmid. RT-PCR and ELISA were used to confirm the expression of VEGF165-PE38
in the transfected hMSCs-like cells. These cells released 1390 ± 137 pg VEGF165-PE38/104cells over 48 h into the culture medium and the supernatant was capable of selectively killing human umbilical vein endothelial
cells (HUVECs) and increasing apoptosis in these cells. In contrast, RPMI8226 was not inhibited by identical supernatants.
Thus, these results lay the foundation for further studies on the potential role of hMSCs-like cells as a targeted therapeutic
delivery vehicle for immunotoxins.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. 相似文献
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WeiWei Wang Wei Wang Yan Jiang Zezheng Li Jin Cheng Nanmei Liu GuoFeng Han Shi Lu JinYuan Zhang 《Biotechnology letters》2014,36(3):667-676
Human adipose-derived stem cells (hASCs) improve renal function in acute kidney injury. Hypoxia-inducible factor-1α (HIF-1α) was transfected into hASCs. hASCs modified by lentivirus-mediated empty-vector and HIF-1α maintained their stem cell characteristics. The expression of the renal-protective gene, heme oxygenase-1 and vascular endothelial growth factor were significantly increased in hASCs modified by HIF-1α, compared to hASCs modified by empty-vector. Cellular ultra-structure and TUNEL staining revealed that hASCs modified by HIF-1α promoted the recovery of apoptotic morphology in cisplatin-treated human kidney-2 cells (HK-2 cells) when compared to hASCs modified by empty-vector. Additionally, hASCs modified by empty-vector inhibited caspase-3 expression and up-regulated Bcl-2 expression in cisplatin-treated HK-2 cells, an effect even more pronounced with hASCs modified by HIF-1α. Thus, HIF-1α gene-modified ASCs could be an effective way to enhance the renal-protective effect. 相似文献