Objective

Mesenchymal stem cells (MSCs) can differentiate into chondroblasts, adipocytes, or osteoblasts under appropriate stimulation. Ghrelin, an endogenous ligand for the growth hormone secretagogue receptor (GHSR), stimulates growth hormone (GH) secretion and exerts both orexigenic and adipogenic effects. The ERK1/2 signaling pathway is known to trigger osteogenic differentiation of rabbit bone marrow-derived mesenchymal stromal cells. In the present study, the function of miR-206 in the ghrelin-mediated osteogenic differentiation of rabbit bone marrow-derived mesenchymal stromal cells (rMSCs) was explored.

Methods

The expression of miR-206 was detected by qPCR, and phosphorylated ERK1/2 and the protein expression levels of ALP, RUNX2, and Osterix were assessed by western blotting. Results: Ghrelin inhibited the expression of miR-206 to promote the osteogenic differentiation of rMSCs. Moreover, ghrelin increased the phosphorylation of ERK1/2, while overexpression of miR-206 suppressed ERK1/2 phosphorylation, indicating that miR-206 can regulate the ERK1/2 pathway. Further, inhibition of ERK1/2 had no influence on miR-206 expression; however, the phosphorylation of ERK1/2 was decreased, and the protein expression levels of ALP, RUNX2, and Osterix were downregulated. Conclusions: Ghrelin promotes the osteogenic differentiation of rMSCs via miR-206 and the ERK1/2 pathway.

中文翻译：

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Ghrelin 通过 miR-206 和 ERK1/2 通路促进 rMSCs 的成骨分化。

客观的

间充质干细胞 (MSCs) 在适当的刺激下可以分化为成软骨细胞、脂肪细胞或成骨细胞。Ghrelin 是生长激素促分泌素受体 (GHSR) 的内源性配体，可刺激生长激素 (GH) 分泌并发挥促食欲和脂肪生成作用。已知 ERK1/2 信号通路可触发兔骨髓间充质基质细胞的成骨分化。在本研究中，研究了 miR-206 在兔骨髓间充质基质细胞 (rMSCs) 生长激素释放肽介导的成骨分化中的作用。

方法

通过qPCR检测miR-206的表达，并通过蛋白质印迹评估磷酸化的ERK1/2和ALP、RUNX2和Osterix的蛋白表达水平。结果：Ghrelin通过抑制miR-206的表达促进rMSCs的成骨分化。此外，ghrelin 增加了 ERK1/2 的磷酸化，而 miR-206 的过表达抑制了 ERK1/2 的磷酸化，表明 miR-206 可以调节 ERK1/2 通路。此外，抑制 ERK1/2 对 miR-206 表达没有影响；然而，ERK1/2的磷酸化降低，ALP、RUNX2和Osterix的蛋白表达水平下调。结论：Ghrelin 通过 miR-206 和 ERK1/2 通路促进 rMSCs 的成骨分化。