Therapeutic Properties of Mesenchymal Stem Cell on Organ Ischemia-reperfusion Injury: A Review

2021 ◽  
pp. 83-102
Author(s):  
Joan Oliva
Keyword(s):  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Therapeutic Properties

scholarly journals Bone marrow mesenchymal stem cell-secreted exosomes carrying microRNA-125b protect against myocardial ischemia reperfusion injury via targeting SIRT7

2019 ◽  
Vol 465 (1-2) ◽  
pp. 103-114 ◽  
Author(s):  
Qi Chen ◽  
Yu Liu ◽  
Xueyan Ding ◽  
Qinfeng Li ◽  
Fuyu Qiu ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Myocardial Ischemia ◽  
Western Blot ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

AbstractMicroRNA-125b (miR-125b) reduces myocardial infarct area and restrains myocardial ischemia reperfusion injury (I/R). In this study, we aimed to investigate the effect of bone marrow mesenchymal stem cell (BMSC)-derived exosomes carrying miR-125b on I/R rats. The myocardial I/R model in rats was constructed by ligation of the left anterior descending coronary artery (LAD). Rats were randomly divided into I/R and Sham group. Lv-cel-miR-67 (control) or Lv-miR-125b was transfected into BMSCs. Exosomes were extracted from transfected BMSCs, and separately named BMSC-Exo-67, BMSC-Exo-125b, and BMSC-Exo. MTT assay and flow cytometry were used to detect the viability and apoptosis of I/R myocardium cells, respectively. The expression of cell apoptosis proteins and the levels of inflammatory factors were examined by Western blot and ELISA assay, respectively. The target relationship between miR-125b and SIRT7 was predicted by using StarBase3.0, and was confirmed by using dual-luciferase reporter gene assay. qRT-PCR, immunohistochemistry staining, and Western blot were used to evaluate the expression of SIRT7 in myocardium tissues in I/R rats. BMSC-derived exosomes were successfully isolated and identified by TEM and positive expression of CD9 and CD63. The expression of miR-125b was down-regulated in I/R myocardium tissues and cells. BMSC-Exo-125b significantly up-regulated miR-125b in I/R myocardium cells. The intervention of BMSC-Exo-125b significantly increased the cell viability, decreased the apoptotic ratio, down-regulated Bax and caspase-3, up-regulated Bcl-2, and decreased the levels of IL-1β, IL-6, and TNF-α in I/R myocardium cells. SIRT7 was a target of miR-125b, and BMSC-Exo-125b significantly down-regulated SIRT7 in myocardium cells. In addition, the injection of BMSC-Exo-125b alleviated the pathological damages and down-regulated SIRT7 in myocardium tissues of I/R rats. BMSC-derived exosomes carrying miR-125b protected against myocardial I/R by targeting SIRT7.

Human Mesenchymal Stem Cell-derived Exosomes Reduce Ischemia/Reperfusion Injury by the Inhibitions of Apoptosis and Autophagy

2019 ◽  
Vol 24 (44) ◽  
pp. 5334-5341 ◽  
Author(s):  
Xiaofei Jiang ◽  
Kar-Sheng Lew ◽  
Qiying Chen ◽  
Arthur M. Richards ◽  
Peipei Wang
Keyword(s):  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Cell Viability ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Human Mesenchymal Stem Cell ◽  
Ldh Release ◽  
Induced Apoptosis

Background: Human mesenchymal stem cell-derived exosomes (hMSC-Exo) have been shown to reduce ischemia/reperfusion injury (I/R) in multiple models. I/R-induced apoptosis or autophagy play important roles in cell death. However, little or no reports demonstrate any roles of hMSC-Exo in this regards. Objective: To test the hypothesis that the inhibition of I/R-induced apoptosis and autophagy play a pivotal role in the cardioprotection of hMSC-Exo. Methods: Myoblast H9c2 cells and isolated rat hearts underwent hypoxia/re-oxygenate (H/R) or ischemia/ reperfusion (I/R) respectively. H9c2 were treated with 1.0 μg/ml Exo, in comparison with 3-MA or rapamycin (Rapa), a known anti- or pro-autophagic agent respectively. Hearts were treated with 0.5, 1.0 and 2.0 μg/ml Exo for 20 min in the beginning of reperfusion. Cell viability, WST assay, LDH release, Annexin-V staining apoptosis assay and GFP-LC3 labeled autophagosomes formation, cardiac function and Western blot were measured. Results: Exo significantly reduced H/R injury as indicated by increased cell viability and reduced LDH and apoptosis. 3-MA, while Rapa, showed increased or decreased protective effects. Rapa-induced injury was partially blocked by Exo. Exo decreased LC3-II/I ratio and increased p62, inhibited autophagosome formation, an indication of autophagy inhibition. In isolated heart, Exo increased cardiac functional recovery and reduced LDH release in I/R. Bcl-2 was significantly upregulated by Exo but not 3-MA. Exo downregulated Traf6 and upregulated mTORC1/p-4eBP1. Conclusion: Exo reduce I/R-induced apoptosis and autophagy. Up-regulation of Bcl-2 is the cross-talk between these two processes. The down-regulation of Traf6 and activation of mTORC1 are additional mechanisms in the inhibition of apoptosis and autophagy.

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