Welcome to our first *functional* post of the new website blog. Rather than making this a generic post - I thought I would write about some of the more unknown peptides which I feel will be of great help in the life sciences field in the near future.

One peptide which I have researched a fair amount, is called MOTS-C. There are numerous studies out there showing the many different ways this peptide has been bringing about some remarkable results after various clinical trials in vitro and in vivo, and below is a copy & paste of the abstract of one such study.

Credit to: F-B Weng , L-F Zhu, J-X Zhou, Y Shan, Z-G Tian, L-W Yang courtesy of: 

Department of Orthopedics, The Ninth People's Hospital of Suzhou, Suzhou, China. 




You can read the article by visiting PMID: 31858528

Objective: To elucidate the function of MOTS-c in accelerating bone fracture healing by inducing BMSCs differentiation into osteoblasts, as well as its potential mechanism.


Materials and methods: Primary BMSCs were extracted from rats and induced for osteogenesis. The highest dose of MOTS-c that did not affect BMSCs proliferation was determined by CCK-8 assay. After 7-day osteogenesis, the relative levels of ALP, Bglap, and Runx2 in MOTS-c-treated BMSCs influenced by FOXF1 were examined. ALP staining and alizarin red S staining in BMSCs were performed as well. The interaction between FOXF1 and TGF-β was analyzed by ChIP assay. At last, rescue experiments were performed to uncover the role of FOXF1/TGF-β axis in MOTS-c-induced osteogenesis.


Results: 1 μM MOTS-c was the highest dose that did not affect BMSCs proliferation. MOTS-c treatment upregulated the relative levels of ALP, Bglap, and Runx2, and stimulated mineralization ability in BMSCs, which were attenuated by the silence of FOXF1. TGF-β was proved to interact with FOXF1, and its level was positively mediated by FOXF1. The silence of FOXF1 attenuated the accelerated osteogenesis and TGF-β upregulation in BMSCs because of MOTS-c induction, and these trends were further reversed by the overexpression of TGF-β.


Conclusions: MOTS-c treatment markedly induces osteogenesis in BMSCs. During MOTS-c-induced osteogenic progression, the upregulated FOXF1 triggers the activation of TGF-β pathway, thus accelerating bone fracture healing.

 

This is one of a few studies out there showing the remarkable effects of this peptide. I am writing this as a first post to test the website but rest assured I have much more info to post very shortly!


Wade