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

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

  • Eur Rev Med Pharmacol Sci. 2019 Apr;23(8):3183-3189. doi: 10.26355/eurrev_201904_17676.
N Che 1,  W Qiu,  J-K Wang,  X-X Sun,  L-X Xu,  R Liu,  L Gu
Affiliations

Affiliation

  • 1 Department of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China. hnjsycwxd@163.com.
PMID: 31081069 DOI: 10.26355/eurrev_201904_17676
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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