Mitochondrial ROS-K+ channel signaling pathway regulated secretion of human pulmonary artery endothelial cells

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 (40 μM) induced HPAEC mitochondrial generation of ROS, rotenone (2 μmol/L...

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Bibliographic Details
Published in:Free radical research 2012-12, Vol.46 (12), p.1437-1445
Main Authors: Ouyang, Jin-Sheng, Li, Yu-Ping, Li, Cheng-Ye, Cai, Chang, Chen, Cheng-Shui, Chen, Shao-Xian, Chen, Yan-Fan, Yang, Li, Xie, Yu-Peng
Format: Article
Language:English
Subjects:
Acrolein - pharmacology
Blotting, Western
Calcium - metabolism
Cell Proliferation - drug effects
Cells, Cultured
cytokines
endothelial dysfunction
Endothelin-1 - genetics
Endothelin-1 - metabolism
Endothelium, Vascular - cytology
Endothelium, Vascular - drug effects
Endothelium, Vascular - metabolism
Enzyme-Linked Immunosorbent Assay
Humans
Hydrogen Peroxide - metabolism
Kv1.5 Potassium Channel - genetics
Kv1.5 Potassium Channel - metabolism
membrane potential
Membrane Potential, Mitochondrial - drug effects
mitochondria
Mitochondria - drug effects
Mitochondria - metabolism
Nitric Oxide Synthase - genetics
Nitric Oxide Synthase - metabolism
Oxidative Stress - drug effects
potassium channel
Pulmonary Artery - cytology
Pulmonary Artery - drug effects
Pulmonary Artery - metabolism
reactive oxygen species
Reactive Oxygen Species - metabolism
Real-Time Polymerase Chain Reaction
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - genetics
Rotenone - pharmacology
Signal Transduction
Uncoupling Agents - pharmacology
Vascular Endothelial Growth Factor A - genetics
Vascular Endothelial Growth Factor A - metabolism
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Summary: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 (40 μM) induced HPAEC mitochondrial generation of ROS, rotenone (2 μmol/L) blocked mitochondrial respiratory chain complex I, cesium chloride (CsCl, 40 mmol/L)blocked K+channels, and saline (0.9 g/dl) were used as control. The generations of NOS, ET-1 and VEGF were determined with ELISA in the condition of different treatment reagents namely acrolein, acrolein plus rotenone, acrolein plus CsCl and saline. In the different 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.
ISSN:1071-5762
1029-2470
DOI:10.3109/10715762.2012.724532