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Researchers from Peking University First Hospital and Wuhan Children’s Hospital of Hubei Province published a titled "Persulfidation of transcription factor FOXO1 at cysteine 457: A novel mechanism by which H 2 S " in the Journal of Advanced Research (IF: 10.
Screenshot of the paper
The abnormal proliferation of VSMC is involved in the pathogenesis of a variety of vascular injury diseases.
Schematic diagram of the oversulfide modification mechanism of endogenous hydrogen sulfide inhibiting the proliferation of vascular smooth muscle cells
In order to clarify the regulatory mechanism of endogenous H 2 S on vascular smooth muscle cells, studies have found that H 2 S can inhibit endothelin-1 (ET-1)-induced cell proliferation through FOXO1, that is, when ET-1 is administered After promoting cell proliferation, the H 2 S donor NaHS can block the increase in phosphorylated FOXO1 level caused by ET-1, inhibit the transfer of FOXO1 from the nucleus to the cytoplasm, and significantly inhibit cell proliferation
The study found that the 457th cysteine (cysteine 457, Cys457) of the FOXO1 molecule is highly conserved among different species through the sequence alignment analysis of FOXO1 from different species, and the Cys457 site is located in the transcriptional activation region (421-655aa) of FOXO1.
In summary, this study found that H 2 S modifies the 457th cysteine of transcription factor FOXO1 by oversulfurization, inhibits the inactivation of FOXO1 phosphorylation-dependent FOXO1 pathway, and blocks the proliferation factor-induced VSMC proliferation