分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

MOTS-c improves osteoporosis by promoting the synthesis of type I collagen in osteoblasts via TGF-β/SMAD signaling pathway

N. Che, W. Qiu, J.-K. Wang, X.-X. Sun, L.-X. Xu, R. Liu, L. Gu

Journal:European Review for Medical and Pharmacological Sciences

IF:2.72

DOI:10.26355/eurrev_201904_17676

PMID:31081069

Published:2019-04-30

research field:分子生物学免疫学心血管疾病信号转导

Abstract

OBJECTIVE: To investigate whether MOTS-c can regulate the synthesis of type I collagen in osteoblasts by regulating TGF-β/SMAD pathway, thereby improving osteoporosis. MATERIALS AND METHODS: Viability of hFOB1.19 cells treated with MOTS-c was detected by CCK-8 assay. The mRNA and protein levels of TGF-β, SMAD7, COL1A1 and COL1A2 in hFOB1.19 cells were detected by quantitative Real-time polymerase chain reaction (qRT-PCR) and Western blot, respectively. We then changed expressions of TGF-β and SMAD7 by plasmids transfection to detect levels of COL1A1 and COL1A2 in hFOB1.19 cells by qRT-PCR and Western blot, respectively. RESULTS: Cell viability was significantly increased after treatment of 1.0 μM MOTS-c for 24 h or 0.5 μM MOTS-c for 48 h in a time-dependent manner. The mRNA and protein expressions of TGF-β, SMAD7, COL1A1 and COL1A2 in hFOB1.19 cells were dependent on the concentration of MOTS-c. In addition, MOTS-c increased the expressions of COL1A1 and COL1A2, which were partially reversed by knockdown of TGF-β or SMAD7. CONCLUSIONS: MOTS-c could promote osteoblasts to synthesize type I collagen via TGF-β/SMAD pathway.

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