Hydrogen sulfide rescues high glucose-induced migration dysfunction in HUVECs by upregulating miR-126-3p.

摘要: Diabetes (especially Type II) is one of the primary threats to cardiovascular health. Wound healing defects and vascular dysfunction are common in diabetic patients, cause deterioration sustained high plasma glucose. microRNA, a noncoding RNA, has regulatory functions that critical maintaining homeostasis. MicroRNA (miR)-126-3p potential diabetes biomarker proangiogenic factor, its level decreases patients. Previous studies have revealed character gasotransmitter hydrogen sulfide (H2S). However, little known about relationship between H2S miR-126-3p when extracellular glucose high, let alone their influences on deteriorated endothelial cell migration, key component angiogenesis, which crucial for wound healing. Human umbilical vein cells (HUVECs) were treated with (33.3 mmol/L) or normal (5.5 48 h. Affymetrix miRNA profiling real-time PCR used validate expression. An probe (HSip-1) was detect endogenous H2S. Scratch wound-healing assays evaluate HUVEC migration. The protein levels quantified by Western blot. Both exogenous could upregulate HUVECs muscle tissue. High decreased expression H2S-producing enzyme cystathionine γ-lyase (CSE) HUVECs; however, DNA methyltransferase 1 (DNMT1) upregulated. CSE overexpression not only increased decreasing DNMT1 but also rescued migration inhibited HUVECs, whereas silencing improved expression, thus inducing HUVECs. Treatment endogenously produced would rescue this through H2S-DNMT1-miR-126-3p.