Mots-C
Mitochondrial open reading frame of the 12S rRNA-c, MT-RNR1, Mitochondrial-derived peptide MOTS-c
MOTS-c improves osteoporosis by promoting the synthesis of type I collagen in osteoblasts via TGF-β/SMAD signaling pathway.
Che. N N; Qiu. W W; Wang. J-K JK; Sun. X-X XX; Xu. L-X LX; Liu. R R; Gu. L L
Key Findings
- MOTS‑c increased viability of osteoblast‑like hFOB1.19 cells at 0.5‑1.0 µM.
- MOTS‑c dose‑dependently raised mRNA and protein levels of TGF‑β, SMAD7, COL1A1 and COL1A2.
- Knocking down TGF‑β or SMAD7 partially blocked the MOTS‑c‑induced rise in COL1A1 and COL1A2, confirming the pathway involvement.
Practical Outcomes
- For biohackers interested in bone health, MOTS‑c shows promise as a molecule that could stimulate collagen production in bone cells, but the evidence is limited to cell culture. No human dosing, safety, or efficacy data are available yet, so it cannot be recommended for self‑administration. Future research (animal and clinical trials) will be needed before it can be incorporated into any real‑world bone‑strengthening protocol.
Summary
A lab study found that the peptide MOTS‑c can boost the production of type I collagen in human bone‑forming cells by activating the TGF‑β/SMAD signaling pathway, which could help improve bone strength and counter osteoporosis. The effect was seen at low micromolar concentrations and depended on the amount of peptide used.
Abstract
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.
Study Information
pubmed
2019
2019-04-01T00:00:00.000Z
10.26355/eurrev_201904_17676
18
24