MiR-146a inhibits proliferation and induces apoptosis in murine osteoblastic MC3T3-E1 by regulating Bcl2.

Autor:	Zhang B; Department of Orthopedics, Shuyang Hospital of Traditional Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Suqian, China. zhangbinsy@126.com., Yi J, Zhang CL, Zhang QH, Xu JF, Shen HQ, Ge DW
Jazyk:	angličtina
Zdroj:	European review for medical and pharmacological sciences [Eur Rev Med Pharmacol Sci] 2017 Oct; Vol. 21 (17), pp. 3754-3762.
Abstrakt:	Objective: The dysregulation of proliferation and apoptosis plays a significant role in the pathogenesis of hormone-induced osteonecrosis of femoral head (ONFH). The research aimed to explore the regulatory role of miR-146a in dexamethasone (DEX)-induced proliferation and apoptosis change in MC3T3-E1 cells from murine osteoblastic. Material and Methods: In this study, MC3T3-E1 was co-cultured with 10-7 DEX for 6 h, then RT-PCR was employed to test the expression level of miR-146a and Bcl2. CCK8 assay and flow cytometry were adopted to verify miR-146a could regulate proliferation and apoptosis. After transfected MC3T3-E1 with mimics and inhibitor, RT-PCR and Western blot was used to detect Bcl2 expression level. Results: In DEX treated MC3T3-E1 cells showed higher MiR-146a expression level and lower Bcl2 expression level. MiR-146a could inhibit proliferation and promotes apoptosis in murine osteoblastic MC3T3-E1 cells. Additionally, Bcl2 gene is regulated by MiR-146a. Conclusions: The MiR-146a expression level increased, while Bcl2 has low expression level in dexamethasone treated MC3T3-E1 cells. MiR-146a regulates proliferation and apoptosis of mouse bone cells. The low expression level of Bcl2 in DEX treated MC3T3-E1 cells is caused by increased MiR-146a level.
Databáze:	MEDLINE
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