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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 저널정보
- 대한약리학회 The Korean Journal of Physiology & Pharmacology The Korean Journal of Physiology & Pharmacology 제25권 제2호
- 발행연도
- 2021.1
- 수록면
- 159 - 166 (8page)
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Nicotinamide adenine dinucleotide phosphate oxidases (NOXs) are the major enzymatic source of reactive oxygen species (ROS). NOX2 and NOX4 are expressed in the heart but its role in hypoxia-induced atrial natriuretic peptide (ANP) secretion is unclear. This study investigated the effect of NOX on ANP secretion induced by hypoxia in isolated beating rat atria. The results showed that hypoxia significantly upregulated NOX4 but not NOX2 expression, which was completely abolished by endothelin-1 (ET-1) type A and B receptor antagonists BQ123 (0.3 ?M) and BQ788 (0.3 ?M). ET-1-upregulated NOX4 expression was also blocked by antagonists of secreted phospholipase A2 (sPLA2; varespladib, 5.0 ?M) and cytosolic PLA2 (cPLA2; CAY10650, 120.0 nM), and ET-1-induced cPLA2 expression was inhibited by varespladib under normoxia. Moreover, hypoxia-increased ANP secretion was evidently attenuated by the NOX4 antagonist GLX351322 (35.0 ?M) and inhibitor of ROS N-Acetyl-D-cysteine (NAC, 15.0 mM), and hypoxia-increased production of ROS was blocked by GLX351322. In addition, hypoxia markedly upregulated Src expression, which was blocked by ET receptors, NOX4, and ROS antagonists. ET-1-increased Src expression was also inhibited by NAC under normoxia. Furthermore, hypoxiaactivated extracellular signal-regulated kinase 1/2 (ERK1/2) and protein kinase B (Akt) were completely abolished by Src inhibitor 1 (1.0 ?M), and hypoxia-increased GATA4 was inhibited by the ERK1/2 and Akt antagonists PD98059 (10.0 ?M) and LY294002 (10.0 ?M), respectively. However, hypoxia-induced ANP secretion was substantially inhibited by Src inhibitor. These results indicate that NOX4/Src modulated by ET-1 regulates ANP secretion by activating ERK1/2 and Akt/GATA4 signaling in isolated beating rat hypoxic atria
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참고문헌 (25)
참고문헌 신청
Zhang Y / 2020 / NADPH oxidases and oxidase crosstalk in cardiovascular diseases : novel therapeutic targets / Nat Rev Cardiol 17:170~194
Zhang M / 2013 / NADPH oxidases in heart failure: poachers or gamekeepers? / Antioxid Redox Signal 18:1024~1041
Bedard K / 2007 / The NOX family of ROS-generating NADPH oxidases : physiology and pathophysiology / Physiol Rev 87:245~313
Bendall JK / 2002 / Pivotal role of a gp91(phox)-containing NADPH oxidase in angiotensin II-induced cardiac hypertrophy in mice / Circulation 105:293~296
Rodiño-Janeiro BK / 2013 / Current status of NADPH oxidase research in cardiovascular pharmacology / Vasc Health Risk Manag 9:401~428
Zhang M / 2013 / NADPH oxidases in heart failure: poachers or gamekeepers? / Antioxid Redox Signal 18:1024~1041
Bedard K / 2007 / The NOX family of ROS-generating NADPH oxidases : physiology and pathophysiology / Physiol Rev 87:245~313
Bendall JK / 2002 / Pivotal role of a gp91(phox)-containing NADPH oxidase in angiotensin II-induced cardiac hypertrophy in mice / Circulation 105:293~296
Rodiño-Janeiro BK / 2013 / Current status of NADPH oxidase research in cardiovascular pharmacology / Vasc Health Risk Manag 9:401~428
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