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- W2991290036 abstract "Mesenchymal stem cells (MSCs) are under consideration for myocardial ischemia-reperfusion (I/R) injury therapy, but their mechanism remains to be evaluated. In this article, we aimed to study the effects of the miR-29a/follistatin-like 1 axis in bone marrow–derived mesenchymal stem cells on modulating myocyte apoptosis after hypoxia-reoxygenation (H/R) injury. An in vitro myocardial ischemia-reperfusion injury model of H9c2 cells was developed by hypoxia-reoxygenation injury. The mRNA levels of follistatin-like 1, Bcl-2, Bax, and miR-29a and the protein levels of Bcl-2, Bax, cleaved caspase-3, and components of the JAK2/STAT3 pathway were detected by qRT-PCR and western blotting, respectively. Secretion of follistatin-like 1 was evaluated by enzyme-linked immunosorbent assay. Cell apoptosis was evaluated by flow cytometry. The interaction between miR-29a and follistatin-like 1 was evaluated by dual luciferase reporter assay. MiR-29a suppressed the expression and secretion of follistatin-like 1 in bone marrow–derived mesenchymal stem cells. Overexpression of follistatin-like 1 in bone marrow–derived mesenchymal stem cells decreased apoptosis of myocytes induced by hypoxia-reoxygenation. Cell apoptosis in myocytes was promoted by conditioned medium from bone marrow–derived mesenchymal stem cells with ectopic miR-29a expression. Conditioned medium of miR-29a-overexpressing bone marrow–derived mesenchymal stem cells inhibited the JAK2/STAT3 pathway in myocytes to promote apoptosis of myocytes. MiR-29a in bone marrow–derived mesenchymal stem cells inhibits follistatin-like 1 secretion and promotes myocyte apoptosis by suppressing the JAK2/STAT3 pathway in hypoxia-reoxygenation injury." @default.
- W2991290036 created "2019-12-05" @default.
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- W2991290036 date "2020-05-01" @default.
- W2991290036 modified "2023-10-16" @default.
- W2991290036 title "MiR-29a in mesenchymal stem cells inhibits FSTL1 secretion and promotes cardiac myocyte apoptosis in hypoxia-reoxygenation injury" @default.
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- W2991290036 doi "https://doi.org/10.1016/j.carpath.2019.107180" @default.
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