MiR-1301 promotes adipogenic and osteogenic differentiation of BMSCs by targeting Satb2.

运行x2 脂肪生成 下调和上调 转染 细胞生长 间充质干细胞 免疫印迹 化学 细胞 细胞生物学 男科 分子生物学 细胞培养 生物 基因表达 医学 基因 生物化学 遗传学
作者
Jing Kong,L-P Wan,Z-M Liu,S-T Gao
出处
期刊:European Review for Medical and Pharmacological Sciences 卷期号:24 (7): 3501-3508 被引量:2
标识
DOI:10.26355/eurrev_202004_20809
摘要

OBJECTIVE Bone marrow mesenchymal stem cells (BMSCs) have the ability to differentiate into several cell lines and are critical for skeletal microenvironment and bone development. MiR-1301 is involved in multiple pathological and physiological processes. However, miR-1301's role in BMSCs adipogenic and osteogenic differentiation remains unclear. MATERIALS AND METHODS Rat BMSCs were isolated and randomly divided into control group, miR-1301 group, and miR-1301 siRNA group followed by analysis of the expression of miR-1301, Bax, Bcl-2, UNX2, and OPN, as well as FABP4 and PPARγ2 by Real Time-PCR. Cell proliferation was assessed by MTT assay and the relationship between miR-1301 and Satb2 was evaluated by the Dual-Luciferase reporter assay. Satb2 expression was detected by Western blot. RESULTS The pcDNA-miR-1301 plasmid was transfected into BMSCs to upregulate the expression of miR-1301, which promoted cell proliferation, decreased Bax expression, and increased Bcl-2 expression and ALP activity. In addition, it also elevated the expression of RUNX2 and OPN and decreased the expression of FABP4, PPARγ2, and Satb2. Compared with the control group, the difference was statistically significant (p<0.05); Satb2 was the target gene of miR-1301. MiR-1301 siRNA transfected into BMSCs down-regulated miR-1301 expression, inhibited cell proliferation, increased Bax expression and decreased Bcl-2 expression and ALP activity. Meanwhile, miR-1301 siRNA also reduced RUNX2 and OPN expression and increased expression of FABP4, PPARγ2 and Satb2. The difference was statistically significant compared with control group (p<0.05). CONCLUSIONS Regulation of miR-1301 expression in BMSCs can improve BMSCs proliferation and regulate their adipogenic and osteogenic differentiation by regulating Satb2.
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