Abstract
AimVascular smooth muscle cell (VSMC) proliferation in response to hyperglycemia is an important process in the development of arterial vessel hyperplasia. The shape change of mitochondria is dynamic and closely related to fission and fusion. Hydrogen sulfide (H2S) was confirmed to have anti-oxidative, anti-inflammatory and anti-proliferative effects. However, little it is known about its effects on mitochondrial morphology induced by hyperglycemia. The aim of the study is to demonstrate that H2S inhibits VSMC proliferation through regulating mitochondrial fission.Methods and resultsWe observe lower H2S levels as well as higher proliferative protein expression levels for proliferative cell nuclear antigen (PCNA) and cyclin D1 and higher mitochondrial fusion–fission protein expression levels for dynamin-related protein 1 (Drp 1) in human kidney arteries and in db/db mouse aorta. Exogenous H2S (100 μM NaHS) inhibits vascular smooth muscle cells of human pulmonary aorta(HPASMC) proliferation and migration in response to high glucose using the BrdU and scratch wound repair assays, decreases proliferative protein (PCNA and cyclin D1) expression, and reduces ROS production in the cytoplasm and mitochondria. When HPASMCs proliferate with a high glucose treatment, the mitochondria become small spheres with a short rod-shaped structure, whereas NaHS, a mitochondrial division inhibitor and siDrp prevent VSMC proliferation and maintain mitochondria as stationary and randomly dispersed with fixed structures.ConclusionExogenous H2S aids in inhibiting mitochondrial fragmentation and affects proliferation in db/db mice and HPASMCs by decreasing Drp 1 expression.Electronic supplementary materialThe online version of this article (doi:10.1186/s13578-016-0102-x) contains supplementary material, which is available to authorized users.
Highlights
Diabetes mellitus is one of the most dangerous factors for cardiovascular disease
hydrogen sulfide (H2S) levels and associated proliferation protein expression levels in human renal arteries from type 2 diabetes patients and db/db mice Some studies have demonstrated that chronic hyperglycemia has been shown to stimulate HPASMC proliferation and migration [19]
We found that proliferative cell nuclear antigen (PCNA) and Cyclin D1 protein expression increased, whereas P27 expression decreased in renal arteries from type 2 diabetes patients (Fig. 1a)
Summary
Diabetes mellitus is one of the most dangerous factors for cardiovascular disease. Atherosclerosis and post-percutaneous coronary intervention induce VSMC injury; VSMCs lose contractile function and convert to Mitochondria control virtually every aspect of cell function via changing the ATP concentration, contributing to Ca2+ signaling, influencing redox potential, and controlling ROS levels [8, 9]. Mitochondria are dynamic organelles that frequently move, undergo fission and fuse with other mitochondria to maintain their structure and. Mitochondrial fission–fusion can aid in repairing defective mitochondria and plays a role in proper segregation of mitochondria into daughter cells during cell division [10]. Recent studies have demonstrated that, when cells enter a proliferative state, mitochondria become highly dynamic structures. When mitochondrial dynamics are inhibited, VSMCs proliferation is inhibited [11]
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