Mots-C
Mitochondrial open reading frame of the 12S rRNA-c, MT-RNR1, Mitochondrial-derived peptide MOTS-c
MOTS-c improves osteoporosis by promoting osteogenic differentiation of bone marrow mesenchymal stem cells via TGF-β/Smad pathway.
Hu. B-T BT; Chen. W-Z WZ
Key Findings
- MOTS‑c at a non‑toxic dose increased markers of bone cell differentiation (ALP, Bglap, Runx2) in rat BMSCs.
- Treatment led to more calcium nodules and alkaline phosphatase activity, indicating enhanced osteogenesis.
- The TGF‑β/Smad pathway genes were up‑regulated by MOTS‑c, and knocking down TGF‑β1 blocked the bone‑forming effect.
Practical Outcomes
- For biohackers interested in bone health, this study suggests MOTS‑c could be a candidate for supporting bone formation, but the evidence is limited to rat cells in a dish. No human dosage or safety data are available yet, so any self‑experimentation would be highly speculative and should be approached with caution.
Summary
A lab study found that the tiny peptide MOTS‑c can push rat bone‑marrow stem cells to become bone‑forming cells by turning on the TGF‑β/Smad signaling pathway. This boosted calcium deposits in the cells, a sign of stronger bone formation, and the effect disappeared when the key TGF‑β1 gene was blocked.
Abstract
To explore whether MOTS-c could improve osteoporosis by promoting osteogenic differentiation of rat bone mesenchymal stem cells (BMSCs) via transforming growth factor-β (TGF-β)/Smad pathway. Rat BMSCs were isolated and cultured, followed by osteogenic and lipid differentiation. CCK-8 (cell counting kit-8) assay was performed to detect the highest treatment dose of MOTS-c that did not affect cell proliferation. Expressions of osteogenesis-related genes (ALP, Bglap, and Runx2) were detected by qRT-PCR (quantitative Real-Time Polymerase Chain Reaction) and Western blot, respectively. Alizarin red staining and alkaline phosphatase (ALP) cytochemical staining were carried out to evaluate the effect of MOTS-c on BMSCs osteogenesis. TGF-β/Smad pathway-related genes (TGF-β1, TGF-β2, and Smad7) in BMSCs treated with MOTS-c were detected. Finally, TGF-β1 was knocked down to investigate the regulatory effect of MOTS-c on BMSCs osteogenesis. BMSCs exhibited an elongated morphology and was identified with a high purity by flow cytometry. After osteogenic differentiation, alizarin red staining and ALP staining were all positive. MOTS-c treatment could remarkably stimulate the formation of calcified nodules in BMSCs. Besides, TGF-β/Smad pathway-related genes were significantly upregulated after BMSCs were treated with MOTS-c. Promoted osteogenesis by MOTS-c treatment was reversed by the TGF-β1 knockdown. MOTS-c promotes cell differentiation of BMSCs to osteoblasts via TGF-β/Smad pathway.
Study Information
pubmed
2018
2018-11-01T00:00:00.000Z
10.26355/eurrev_201811_16247
33
15