Oxidized low-density lipoprotein inhibits nitric oxide-mediated coronary arteriolar dilation by up-regulating endothelial arginase I.
Oxidized low-density lipoprotein inhibits nitric oxide-mediated coronary arteriolar dilation by up-regulating endothelial arginase I.
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DOI：
10.1111/j.1549-8719.2010.00066.x
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发表时间：
2011-01
期刊：
影响因子：
--
通讯作者：
Kuo L
中科院分区：
文献类型：
--
作者：
Wang W;Hein TW;Zhang C;Zawieja DC;Liao JC;Kuo L
Oxidized low-density lipoprotein (OxLDL) causes impairment of endothelium-dependent, nitric oxide (NO)-mediated vasodilation involving L-arginine deficiency. However, the underlying mechanism remains elusive. Since arginase and endothelial NO synthase (eNOS) share the substrate L-arginine, we hypothesized that OxLDL may reduce L-arginine availability to eNOS for NO production, and thus vasodilation, by up-regulating arginase. To test this hypothesis, porcine subepicardial arterioles (70-130 μm) were isolated for vasomotor study and for immunohistochemical detection of arginase and eNOS expressions. The coronary arterioles dilated dose-dependently to the endothelium-dependent NO-mediated vasodilator serotonin. This vasodilation was inhibited in the same manner by NOS inhibitor L-NAME and by lumenal OxLDL (0.5 mg protein/ml). The inhibitory effect of OxLDL was reversed after treating the vessels with either L-arginine (3 mM) or arginase inhibitor difluoromethylornithine (DFMO; 0.4 mM). Consistent with vasomotor alterations, OxLDL inhibited serotonin-induced NO release from coronary arterioles and this inhibition was reversed by DFMO. Vascular arginase activity was significantly elevated by OxLDL. Immunohistochemical analysis indicated that Ox-LDL increased arginase I expression in the vascular wall without altering eNOS expression. Taken together, these results suggest that OxLDL up-regulates arginase I, which contributes to endothelial dysfunction by reducing L-arginine availability to eNOS for NO production and thus vasodilation.
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DOI：
10.1073/pnas.0603918103
发表时间：
2006-07-05
影响因子：
11.1
作者：
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影响因子：
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DOI：
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发表时间：
1998-01-01
影响因子：
4.8
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影响因子：
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作者：
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影响因子：
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