Abstract
Bone marrow-derived mesenchymal stem cells (MSCs) have shown great promise in tissue engineering and regenerative medicine; however, the regenerative capacity of senescent MSCs is greatly reduced, thus exhibiting limited therapy potential. Previous studies uncovered that microRNA-206 (miR-206) could largely regulate cell functions, including cell proliferation, survival, and apoptosis, but whether miR-206 is involved in the senescent process of MSCs remains unknown. In this study, we mainly elucidated the effects of miR-206 on MSC senescence and the underlying mechanism. We discovered that miR-206 was upregulated in the senescent MSCs induced by H2O2, and abrogation of miR-206 could alleviate this tendency. Besides, we determined that by targeting Alpl, miR-206 could ameliorate the impaired migration and paracrine function in MSCs reduced by H2O2. In vivo study, we revealed that inhibition of miR-206 in senescent MSCs could effectively protect their potential for myocardial infarction treatment in a rat MI model. In summary, we examined that inhibition of miR-206 in MSCs can alleviate H2O2-induced senescence and dysfunction, thus protecting its therapeutic potential.
Highlights
Bone marrow-derived mesenchymal stem cells (MSCs), which can be isolated [1], have been widely studied in tissue engineering and regenerative medicine due to their capacity of immunomodulatory effects, self-renewal, and multilineage differentiation [2]
Flow cytometry showed that the cultured cells were positive for CD90 and CD29 and negative for CD34, CD11b/c, CD86, and CD45 (Figure 1(b)), which was consistent with the surface markers of MSCs
We discovered that the percentage of blue staining cells increased significantly (Figures 2(a) and 2(b)) whereas the percentage of EdU staining cells decreased notably in the H2O2 group than in the NC group (Figures 2(c) and 2(d))
Summary
Bone marrow-derived mesenchymal stem cells (MSCs), which can be isolated [1], have been widely studied in tissue engineering and regenerative medicine due to their capacity of immunomodulatory effects, self-renewal, and multilineage differentiation [2]. They are an optimal candidate in cell therapy strategies due to their feasible and safer properties in regard to the risk of forming tumors and becoming cancerous [3]. Hesari et al have confirmed that upregulation of miR-206 attenuated cell survival and promoted apoptosis in breast cancer
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