AI Article Synopsis
- BMSCs have potential for treating oral and maxillofacial defects, but their effectiveness is hindered by low survival and growth rates.
- The study investigates how miR-31 influences the survival, proliferation, and movement of BMSCs under stress induced by LPS, showing that miR-31 can counteract negative effects and enhance these properties.
- Specifically, miR-31 promotes BMSC survival and growth by inhibiting caspase activation and activates the CXCR4/Akt pathway, which is crucial for its beneficial effects.
Article Abstract
Although bone mesenchymal stem cells (BMSCs) have been used for the treatment of oral and maxillofacial defects, the survival rate and limited proliferation reduces the therapeutic efficiency of BMSC. The aim of our study is to explore the role of miR-31 in regulating survival, proliferation, and migration of BMSC . LPS was used to induce BMSC damage and then miR-31 was used to incubate with BMSC. Subsequently, BMSC proliferation, survival, and migration were determined via ELISA, qPCR, western blots, and immunofluorescence. The expression of miR-31 was downregulated in response to LPS stress. Interestingly, supplementation of miR-31 could reverse the survival, proliferation and migration of BMSC under LPS. Mechanically, miR-31 treatment inhibited the activation of caspase, and thus promoted BMSC survival. Besides, miR-31 upregulated the genes related to cell proliferation, an effect that was followed by an increase in the levels of migratory factors. Further, we found that miR-31 treatment activated the CXCR4/Akt pathway and blockade of CXCR4/Akt could abolish the beneficial effects of miR-31 on BMSC proliferation, survival, and migration. miR-31 could increase the therapeutic efficiency of BMSC via the CXCR4/Akt pathway.
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| http://dx.doi.org/10.1080/10799893.2019.1669054 | DOI Listing |
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