Hydrogen Sulfide Inhibits High Glucose-Induced SFlt-1 Production Via Decreasing ADAM17 Expression in 3T3-L1 Adipocytes
Overview
Affiliations
Hydrogen sulfide (HS) has recently been identified as an endogenous gaseous signaling molecule. The aim of the present study was to investigate the effect of HS on high glucose- (HG-) induced ADAM17 expression and sFlt-1 production in 3T3-L1 adipocytes. Firstly, we found that HG DMEM upregulated the expression of ADAM17 and production of sFlt-1 in 3T3-L1 adipocytes. Knocking down ADAM17 attenuated the effect of high glucose on sFlt-1 production in adipocytes. HG decreased the expression of CSE and 3-MST, as well as the endogenous HS production. Furthermore, knocking down CSE and 3-MST significantly increased ADAM17 expression and sFlt-1 production. The addition of exogenous HS through the administration of sodium hydrosulfide (NaHS) inhibited HG-induced upregulation of ADAM17 expression and sFlt-1 production. In conclusion, decreased expression of CSE and 3-MST and the subsequent decrease in HS production contribute to high glucose-induced sFlt-1 production via activating ADAM17 in adipocytes. Exogenous HS donor NaHS has a potential therapeutic value for diabetic vascular complications.
Implications of pregnancy on cardiometabolic disease risk: preeclampsia and gestational diabetes.
Elgazzaz M, Woodham P, Maher J, Faulkner J Am J Physiol Cell Physiol. 2024; 327(3):C646-C660.
PMID: 39010840 PMC: 11427017. DOI: 10.1152/ajpcell.00293.2024.
Role of 3-Mercaptopyruvate Sulfurtransferase (3-MST) in Physiology and Disease.
Rao S, Dobariya P, Bellamkonda H, More S Antioxidants (Basel). 2023; 12(3).
PMID: 36978851 PMC: 10045210. DOI: 10.3390/antiox12030603.
Pineiro-Ramil M, Burguera E, Hermida-Gomez T, Carames B, Oreiro-Villar N, Meijide-Failde R Antioxidants (Basel). 2022; 11(4).
PMID: 35453313 PMC: 9024787. DOI: 10.3390/antiox11040628.
Hydrogen sulfide modulates high glucose-induced NLRP3 inflammasome activation in 3T3-L1 adipocytes.
Hu T, Zhang N, Ruan Y, Tan Q, Wang J Exp Ther Med. 2019; 19(1):771-776.
PMID: 31885713 PMC: 6913324. DOI: 10.3892/etm.2019.8242.