title: [Expression of KATP in pulmonary artery smooth muscle cells under hypoxia-hypercapnia condition and the relationship with p38 MAPK pathway].
abstract: The aim of the present study is to investigate the expressions of ATP-sensitive K(+) channels (KATP) in pulmonary artery smooth muscle cells (PASMCs) and the relationship with p38 MAPK signal pathway in rats. Male SD rat PASMCs were cultured in vitro, and a model of hypoxia and hypercapnia was reconstructed. PASMCs were divided to normal (N), hypoxia-hypercapnia (H), hypoxia-hypercapnia+DMSO incubation (HD), hypoxia-hypercapnia+SB203580 (inhibitor of p38 MAPK pathway) incubation (HS) and hypoxia-hypercapnia+Anisomycin (agonist of p38 MAPK pathway) incubation (HA) groups. Western blot was used to detect the protein expression of SUR2B and Kir6.1; semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the mRNA expression of SUR2B and Kir6.1. The results demonstrated that: (1) Compared with N, H, HD and HS groups, the expressions of Kir6.1 mRNA and protein in PASMCs of HA group were decreased significantly (P < 0.01), but there were no differences among N, H, HD and HS groups (P > 0.05); (2) Compared with N group, the expressions of SUR2B mRNA and protein in H, HD, HS and HA groups were increased significantly (P < 0.05), but there were no differences among H, HD, HS and HA groups (P > 0.05). The results imply that: (1) Hypoxia-hypercapnia, SB203580 didn't change the expressions of Kir6.1 mRNA and protein in PASMCs, but Anisomycin decreased the expressions of Kir6.1 mRNA and protein, so Kir6.1 may be regulated by the other subfamily of MAPK pathway; (2) Hypoxia-hypercapnia raised SUR2B mRNA and protein expressions in PASMCs, but SB203580 and Anisomycin did not affect the changes, so the increasing of SUR2B mRNA and protein induced by hypoxia-hypercapnia may be not depend on p38 MAPK pathway.
authors: Department of Pathophysiology; Institute of Ischemia/Reperfusion Injury, Wenzhou Medical University, Wenzhou 325035, China; Department of Pathology, Tongde Hospital of Zhejiang Province, Hangzhou 310012, China. wwt@wzmc.edu.cn.
authors: Ying-Chun
authors: YC
authors: Ma
authors: Lin-Jing
authors: LJ
authors: Huang
authors: Meng-Xiao
authors: MX
authors: Zheng
authors: Yuan-Yuan
authors: YY
authors: Wang
authors: Lei
authors: L
authors: Ying
authors: Wan-Tie
authors: WT
authors: Wang
mesh_terms: D000818:Animals; D000841:Anisomycin / Q000494:pharmacology; D015687:Cell Hypoxia; D002478:Cells, Cultured; D006935:Hypercapnia; D007093:Imidazoles / Q000494:pharmacology; D054086:KATP Channels / Q000378:metabolism*; D020935:MAP Kinase Signaling System; D008297:Male; D032389:Myocytes, Smooth Muscle / Q000378:metabolism*; D011651:Pulmonary Artery / Q000166:cytology; D011725:Pyridines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D064233:Sulfonylurea Receptors / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors
chemical_list: C577512:Abcc9 protein, rat; D007093:Imidazoles; D054086:KATP Channels; D011725:Pyridines; D064233:Sulfonylurea Receptors; C092520:uK-ATP-1 potassium channel; D000841:Anisomycin; D048051:p38 Mitogen-Activated Protein Kinases; C093642:SB 203580