贺温州医科大学附属第一医院应用PriCells产品/技术服务发表文章

 

 

 

Jin-Sheng Ouyang , Yu-Ping Li , Cheng-Ye Li , Chang Cai , Cheng-Shui Chen , Shao-Xian Chen ,Yan-Fan Chen , Li Yang & Yu-Peng Xie

 

Department of Respiratory Medicine , The First Affi liated Hospital of Wenzhou Medical College, Wenzhou, China

 

HUM-CELL-0002 \ MED-0002 \ SUP-0002 ,PriCells, Wuhan, China

 

Abstract

The objective was to investigate the molecular mechanism of mitochondrial reactive oxygen species (ROS) signaling regulation of pulmonary artery endothelial cell (HPAEC) secretion in the condition of oxidative stress. Acrolein (40μM) induced HPAEC mitochondrial generation of ROS, rotenone (2μmol/L) blocked mitochondrial respiratory chain complex I, cesium chloride (CsCl, 40mmol/L) blocked K⁺ channels, and saline (0.9g/dl) were used as control. The generations of NOS, ET-1 and VEGF were determined with ELISA in the condition of diff erent treatment reagents namely acrolein, acrolein plus rotenone, acrolein plus CsCl and saline. In the diff erent reagent treatment of HPAECs, acrolein increased mitochondrial ROS, membrane potential, Kv1.5 mRNA and protein expression, intracellular calcium and the generation of NOS (determining NO production), ET-1 and VEGF, and those were reduced by rotenone. CsCl decreased the increment of membrane potential, the elevation of intracellular calcium and the upregulation of NOS, E-1 and VEGF expressions, which were induced by acrolein. The present study demonstrated that mitochondrial ROS-K channel regulated HPAEC secretion of NO, ET-1 and VEGF in the condition of oxidative stress. Kv1.5 channel may be an important component of ROS-K  channel signaling pathway, and intracellular calcium contributed to mitochondrial ROS-K channel signaling modulation of HPAEC secretion.