Abstract:
:Hypoxia-induced arginase elevation plays an essential role in several vascular diseases but influence of arginase on hypoxia-mediated angiogenesis is completely unknown. In this study, in vitro network formation in bovine aortic endothelial cells (BAEC) was examined after exposure to hypoxia for 24h with or without arginase inhibition. Arginase activity, protein levels of the two arginase isoforms, eNOS, and VEGF as well as production of NO and ROS were examined to determine the involvement of arginase in hypoxia-mediated angiogenesis. Hypoxia elevated arginase activity and arginase 2 expression but reduced active p-eNOS(Ser1177) and NO levels in BAEC. In addition, both VEGF protein levels and endothelial elongation and network formation were reduced with continued hypoxia, whereas ROS levels increased and NO levels decreased. Arginase inhibition limited ROS, restored NO formation and VEGF expression, and prevented the reduction of angiogenesis. These results suggest a fundamental role of arginase activity in regulating angiogenic function.
journal_name
Microvasc Resjournal_title
Microvascular researchauthors
Wang L,Bhatta A,Toque HA,Rojas M,Yao L,Xu Z,Patel C,Caldwell RB,Caldwell RWdoi
10.1016/j.mvr.2014.11.002subject
Has Abstractpub_date
2015-03-01 00:00:00pages
1-8eissn
0026-2862issn
1095-9319pii
S0026-2862(14)00170-8journal_volume
98pub_type
杂志文章abstract::Failure of the glomerular barrier causing proteinuria has been modeled chiefly by Chang, Deen, and Brenner. They have refined models from an isoporous filter to a mostly isoporous membrane, which during proteinuric disease opens up nondiscriminating shunts. This report extends these concepts by measuring a larger dist...
journal_title:Microvascular research
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pub_type: 杂志文章
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更新日期:2005-07-01 00:00:00
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pub_type: 杂志文章,随机对照试验
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doi:10.1016/0026-2862(84)90030-x
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