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微小 RNA-132-3p 在循环张应力下抑制 MC3T3-E1 成骨细胞中的 Smad5。

MicroRNA-132-3p represses Smad5 in MC3T3-E1 osteoblastic cells under cyclic tensile stress.

机构信息

Department of Orthodontics, Dental Hospital, Shanxi Medical University, Taiyuan, China.

Suzhou Dental Doctor Outpatient Department Co. LTD, Suzhou, China.

出版信息

Mol Cell Biochem. 2019 Aug;458(1-2):143-157. doi: 10.1007/s11010-019-03538-3. Epub 2019 Apr 19.

Abstract

MicroRNAs (miRNAs) regulate osteogenic differentiation of bone cells, which has applications in orthodontics. Here we evaluated the miRNA expression profile of MC3T3-E1 osteoblasts under cyclic tensile stress with chip technology and found that miR-132-3p was up-regulated by 12% cyclic tensile stress. Alkaline phosphatase activity and osteocalcin expression in MC3T3-E1 cells were decreased under these conditions. Smad2 and Smad5 were identified as potential target genes of miR-132-3p. Native and phosphorylated Smad2 and Smad5 expression was negatively correlated with miR-132-3p levels in the cells under cyclic stretch; however, only Smad5 protein level was reduced upon miR-132-3p overexpression. The luciferase reporter assay confirmed a direct interaction between miR-132-3p and Smad5. Thus, miR-132-3p maybe regulates osteoblast differentiation via Smad5 in response to cyclic tensile stress.

摘要

微小 RNA(miRNAs)调控着骨细胞的成骨分化,这在正畸学中有应用。在这里,我们利用芯片技术评估了 MC3T3-E1 成骨细胞在循环拉伸应力下的 miRNA 表达谱,发现 miR-132-3p 被 12%的循环拉伸应力上调。在这些条件下,MC3T3-E1 细胞中的碱性磷酸酶活性和骨钙素表达下降。Smad2 和 Smad5 被鉴定为 miR-132-3p 的潜在靶基因。在循环拉伸下,细胞中 miR-132-3p 的表达与天然和磷酸化 Smad2 和 Smad5 的表达呈负相关;然而,只有 Smad5 蛋白水平在 miR-132-3p 过表达时降低。荧光素酶报告基因检测证实了 miR-132-3p 与 Smad5 之间的直接相互作用。因此,miR-132-3p 可能通过 Smad5 来调节成骨细胞分化,以响应循环拉伸应力。

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