Effect Of Nuclear Receptor Corepressor On Bone Marrow Mesenchymal Stem Cells Proliferation

Objective: Bone marrow mesenchymal stem cells (BMSCs) are considered a promising cell source for tissue engineering. Methods to advance the proliferation and anti-apoptotic capacity of mesenchymal stem cells (MSCs) are required to improve the efficiency of MSC-based therapy. In this study, we aimed to observe the effect of nuclear receptor corepressor (NCoR) on BMSC proliferation, as well as the relationship between NCoR and insulin. Method: Cells from Wistar rats were isolated, cultured, and transfected with three NCoR small interfering RNA (siRNA), and the most successful sequence was used. After cells were transfected with NCoR siRNA, we estimated cell growth and proliferation using methyl thiazolyl tetrazolium (MTT) and cell growth curve assays. Finally, BMSCs were treated with insulin at various concentrations (0, 5, 15, and 45 mmol/L) before the rate of cell proliferation was examined. Result: The third sequence was the most successful. After MTT assay and cell growth curve assay, NCoR siRNA was shown to inhibit rat BMSC proliferation after 3 days. Insulin at 15 mmol/L remarkably enhanced BMSC proliferation. When the gene NCoR was knocked down from BMSCs, the effect of various insulin concentrations on cell proliferation was inhibited. Conclusion: NCoR siRNA inhibited BMSC growth and proliferation. Insulin could promote BMSC growth and proliferation. After NCoR was knocked out, the effect of insulin on cell proliferation was inhibited. Thus, NCoR inhibited the function of insulin in cell proliferation, and PI3K signaling may play an important role in this event. Future cell studies may seek to investigate the potential underlying mechanism.