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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2021.10
- 수록면
- 516 - 521 (6page)
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초록· 키워드
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Although arginase primarily participates in the last reaction of the urea cycle, we have previously demonstrated that arginase II is an important cytosolic calcium regulator through spermine production in a p32-dependent manner. Here, we demonstrated that rhaponticin (RPT) is a novel medicinal-plant arginase inhibitor and investigated its mechanism of action on Ca2+-dependent endothelial nitric oxide synthase (eNOS) activation. RPT was uncompetitively inhibited for both arginases I and II prepared from mouse liver and kidney. It also inhibited arginase activity in both aorta and human umbilical vein endothelial cells (HUVECs). Using both microscope and FACS analyses, RPT treatments induced increases in cytosolic Ca2+ levels using Fluo-4 AM as a calcium indicator. Increased cytosolic Ca2+ elicited the phosphorylations of both CaMKII and eNOS Ser1177 in a time-dependent manner. RPT incubations also increased intracellular L-arginine (L-Arg) levels and activated the CaMKII/AMPK/Akt/eNOS signaling cascade in HUVECs. Treatment of L-Arg and ABH, arginase inhibitor, increased intracellular Ca2+ concentrations and activated CaMKII-dependent eNOS activation in ECs of WT mice, but, the effects were not observed in ECs of inositol triphosphate receptor type 1 knockout (IP3R1-/-) mice. In the aortic endothelium of WT mice, RPT also augmented nitric oxide (NO) production and attenuated reactive oxygen species (ROS) generation. In a vascular tension assay using RPT-treated aortic tissue, cumulative vasorelaxant responses to acetylcholine (Ach) were enhanced, and phenylephrine (PE)-dependent vasoconstrictive responses were retarded, although sodium nitroprusside and KCl responses were not different. In this study, we present a novel mechanism for RPT, as an arginase inhibitor, to increase cytosolic Ca2+ concentration in a L-Arg-dependent manner and enhance endothelial function through eNOS activation.
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참고문헌 (21)
참고문헌 신청
Ignarro LJ / 2001 / Role of the arginine-nitric oxide pathway in the regulation of vascular smooth muscle cell proliferation / Proc Natl Acad Sci U S A 98:4202~4208
Li H / 2001 / Regulatory role of arginase I and II in nitric oxide, polyamine, and proline syntheses in endothelial cells / Am J Physiol Endocrinol Metab 280:E75~E82
Berkowitz DE / 2003 / Arginase reciprocally regulates nitric oxide synthase activity and contributes to endothelial dysfunction in aging blood vessels / Circulation 108:2000~2006
Hein TW / 2003 / Ischemia-reperfusion selectively impairs nitric oxide-mediated dilation in coronary arterioles : counteracting role of arginase / FASEB J 17:2328~2330
Jung C / 2010 / Arginase inhibition mediates cardioprotection during ischaemia-reperfusion / Cardiovasc Res 85:147~154
Li H / 2001 / Regulatory role of arginase I and II in nitric oxide, polyamine, and proline syntheses in endothelial cells / Am J Physiol Endocrinol Metab 280:E75~E82
Berkowitz DE / 2003 / Arginase reciprocally regulates nitric oxide synthase activity and contributes to endothelial dysfunction in aging blood vessels / Circulation 108:2000~2006
Hein TW / 2003 / Ischemia-reperfusion selectively impairs nitric oxide-mediated dilation in coronary arterioles : counteracting role of arginase / FASEB J 17:2328~2330
Jung C / 2010 / Arginase inhibition mediates cardioprotection during ischaemia-reperfusion / Cardiovasc Res 85:147~154
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