Department of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Eur Rev Med Pharmacol Sci. 2019 Apr;23(8):3183-3189. doi: 10.26355/eurrev_201904_17676.
To investigate whether MOTS-c can regulate the synthesis of type I collagen in osteoblasts by regulating TGF-β/SMAD pathway, thereby improving osteoporosis.
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.
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.
MOTS-c could promote osteoblasts to synthesize type I collagen via TGF-β/SMAD pathway.
通过研究 MOTS-c 是否可以通过调节 TGF-β/SMAD 通路来调节成骨细胞中 I 型胶原的合成，从而改善骨质疏松症。
通过 CCK-8 法检测 MOTS-c 处理的 hFOB1.19 细胞的活力。通过定量实时聚合酶链反应（qRT-PCR）和 Western blot 分别检测 hFOB1.19 细胞中 TGF-β、SMAD7、COL1A1 和 COL1A2 的 mRNA 和蛋白水平。然后，通过质粒转染改变 TGF-β 和 SMAD7 的表达，通过 qRT-PCR 和 Western blot 分别检测 hFOB1.19 细胞中 COL1A1 和 COL1A2 的水平。
MOTS-c 以时间依赖性方式处理 24 小时或 0.5 μM MOTS-c 48 小时后，细胞活力显著增加。hFOB1.19 细胞中 TGF-β、SMAD7、COL1A1 和 COL1A2 的 mRNA 和蛋白表达均依赖于 MOTS-c 的浓度。此外，MOTS-c 增加了 COL1A1 和 COL1A2 的表达，这部分被 TGF-β 或 SMAD7 的敲低所逆转。
MOTS-c 可以通过 TGF-β/SMAD 通路促进成骨细胞合成 I 型胶原。
