Interaction among estrogen, IGF-1, and H2S on smooth muscle cell proliferation

Both estrogen and hydrogen sulfide (H 2 S) inhibit the proliferation of vascular smooth muscle cells (SMCs) development atherosclerosis. In absence endogenous H S as occurred in CSE-knockout (KO) mouse, however, stimulates SMCs. The underlying mechanisms for this seemingly controversial effect are unclear. present study, we demonstrated that stimulatory on CSE-KO SMCs was suppressed by inhibitor insulin-like growth factor-1 receptor (IGF-1R) or knockdown IGF-1R protein expression. Estrogen downregulated expression (IGF-1) aortic tissues isolated from WT mice. Furthermore, IGF-1R, but upregulated (ER)-α, ER-α were co-located co-immunoprecipitated, which decreased S. Finally, both exogenous induced S-sulfhydration not ER-α, WT-SMCs SMCs, underlies formation IGF-1R/ER-α hybrid presence Thus, favors interaction with to stimulate proliferation. appreciation a critical role preventing estrogen-induced will help better understand regulation complex effects sex-related cardiovascular diseases.