Role of PKCζ‐NADPH oxidase signaling axis in PKCα‐mediated Giα2 phosphorylation for inhibition of adenylate cyclase activity by angiotensin II in pulmonary artery smooth muscle cells
| Autor: | Sajal Chakraborti, Tapati Chakraborti, Jaganmay Sarkar, Animesh Chowdhury, Pijush Kanti Pramanik |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Protein Kinase C-alpha Myocytes Smooth Muscle Cell Culture Techniques Adenylate kinase Pulmonary Artery 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Internal medicine medicine Animals Cyclic adenosine monophosphate Phosphorylation Protein kinase A Protein Kinase C NADPH oxidase biology Angiotensin II Isoproterenol NADPH Oxidases Cell Biology General Medicine Adrenergic beta-Agonists GTP-Binding Protein alpha Subunits 030104 developmental biology Endocrinology chemistry 030220 oncology & carcinogenesis cardiovascular system biology.protein Cattle Cyclase activity Nicotinamide adenine dinucleotide phosphate Adenylyl Cyclases Signal Transduction |
| Zdroj: | Cell Biology International. 44:1142-1155 |
| ISSN: | 1095-8355 1065-6995 |
| Popis: | We sought to determine the mechanism by which angiotensin II (AngII) inhibits isoproterenol induced increase in adenylate cyclase (AC) activity and cyclic adenosine monophosphate (cAMP) production in bovine pulmonary artery smooth muscle cells (BPASMCs). Treatment with AngII stimulates protein kinase C-ζ (PKC-ζ), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and PKC-α activities, and also inhibits isoproterenol induced increase in AC activity and cAMP production in the cells. Pertussis toxin pretreatment eliminates AngII caused inhibition of isoproterenol induced increase in AC activity without a discernible change in PKC-ζ, NADPH oxidase, and PKC-α activities. Treatment of the cells with AngII increases α2 isoform of Gi (Giα2) phosphorylation; while pretreatment with chemical and genetic inhibitors of PKC-ζ and NADPH oxidase attenuate AngII induced increase in PKC-α activity and Giα2 phosphorylation, and also reverse AngII caused inhibition of isoproterenol induced increase in AC activity. Pretreatment of the cells with chemical and genetic inhibitors of PKC-α attenuate AngII induced increase in Giα2 phosphorylation and inhibits isoproterenol induced increase in AC activity without a discernible change in PKC-ζ and NADPH oxidase activities. Overall, PKCζ-NADPH oxidase-PKCα signaling axis plays a crucial role in Giα2 phosphorylation resulting in AngII-mediated inhibition of isoproterenol induced increase in AC activity in BPASMCs. |
| Databáze: | OpenAIRE |
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