Hydrogen Sulfide Inhibits High Glucose-Induced sFlt-1 Production via Decreasing ADAM17 Expression in 3T3-L1 Adipocytes

Tian-Xiao Hu; Gang Wang; Wei Wu; Lu Gao; Qing-Ying Tan; Jing Wang

doi:10.1155/2017/9501792

Hydrogen Sulfide Inhibits High Glucose-Induced sFlt-1 Production via Decreasing ADAM17 Expression in 3T3-L1 Adipocytes

Int J Endocrinol. 2017:2017:9501792. doi: 10.1155/2017/9501792. Epub 2017 Jun 27.

Authors

Tian-Xiao Hu¹, Gang Wang², Wei Wu³, Lu Gao², Qing-Ying Tan¹, Jing Wang¹

Affiliations

¹ Department of Endocrinology, Chinese PLA 117th Hospital, Hangzhou 310013, China.
² Department of Physiology, Second Military Medical University, Shanghai 200433, China.
³ Department of Obstetrics and Gynecology, Women's Hospital, School of Medicine, Zhejiang University, Hangzhou 310006, China.

Abstract

Hydrogen sulfide (H₂S) has recently been identified as an endogenous gaseous signaling molecule. The aim of the present study was to investigate the effect of H₂S 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 H₂S production. Furthermore, knocking down CSE and 3-MST significantly increased ADAM17 expression and sFlt-1 production. The addition of exogenous H₂S 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 H₂S production contribute to high glucose-induced sFlt-1 production via activating ADAM17 in adipocytes. Exogenous H₂S donor NaHS has a potential therapeutic value for diabetic vascular complications.