iPLA2β overexpression in smooth muscle exacerbates angiotensin II-induced hypertension and vascular remodeling.

Calcium independent group VIA phospholipase A(2) (iPLA(2)β) is up-regulated in vascular smooth muscle cells in some diseases, but whether the up-regulated iPLA(2)β affects vascular morphology and blood pressure is unknown. The current study addresses this question by evaluating the basal- and angiot...

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Main Authors: Lindsay E Calderon, Shu Liu, Wen Su, Zhongwen Xie, Zhenheng Guo, Wanda Eberhard, Ming C Gong
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2012-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3282780?pdf=render
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author Lindsay E Calderon
Shu Liu
Wen Su
Zhongwen Xie
Zhenheng Guo
Wanda Eberhard
Ming C Gong
author_facet Lindsay E Calderon
Shu Liu
Wen Su
Zhongwen Xie
Zhenheng Guo
Wanda Eberhard
Ming C Gong
author_sort Lindsay E Calderon
collection DOAJ
description Calcium independent group VIA phospholipase A(2) (iPLA(2)β) is up-regulated in vascular smooth muscle cells in some diseases, but whether the up-regulated iPLA(2)β affects vascular morphology and blood pressure is unknown. The current study addresses this question by evaluating the basal- and angiotensin II infusion-induced vascular remodeling and hypertension in smooth muscle specific iPLA(2)β transgenic (iPLA(2)β-Tg) mice.Blood pressure was monitored by radiotelemetry and vascular remodeling was assessed by morphologic analysis. We found that the angiotensin II-induced increase in diastolic pressure was significantly higher in iPLA(2)β-Tg than iPLA(2)β-Wt mice, whereas, the basal blood pressure was not significantly different. The media thickness and media∶lumen ratio of the mesenteric arteries were significantly increased in angiotensin II-infused iPLA(2)β-Tg mice. Analysis revealed no difference in vascular smooth muscle cell proliferation. In contrast, adenovirus-mediated iPLA(2)β overexpression in cultured vascular smooth muscle cells promoted angiotensin II-induced [(3)H]-leucine incorporation, indicating enhanced hypertrophy. Moreover, angiotensin II infusion-induced c-Jun phosphorylation in vascular smooth muscle cells overexpressing iPLA2β to higher levels, which was abolished by inhibition of 12/15 lipoxygenase. In addition, we found that angiotensin II up-regulated the endogenous iPLA(2)β protein in-vitro and in-vivo.The present study reports that iPLA(2)β up-regulation exacerbates angiotensin II-induced vascular smooth muscle cell hypertrophy, vascular remodeling and hypertension via the 12/15 lipoxygenase and c-Jun pathways.
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spelling doaj.art-b199196c0a4741a0b7e650ef2de2af2d2022-12-22T02:27:31ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-0172e3185010.1371/journal.pone.0031850iPLA2β overexpression in smooth muscle exacerbates angiotensin II-induced hypertension and vascular remodeling.Lindsay E CalderonShu LiuWen SuZhongwen XieZhenheng GuoWanda EberhardMing C GongCalcium independent group VIA phospholipase A(2) (iPLA(2)β) is up-regulated in vascular smooth muscle cells in some diseases, but whether the up-regulated iPLA(2)β affects vascular morphology and blood pressure is unknown. The current study addresses this question by evaluating the basal- and angiotensin II infusion-induced vascular remodeling and hypertension in smooth muscle specific iPLA(2)β transgenic (iPLA(2)β-Tg) mice.Blood pressure was monitored by radiotelemetry and vascular remodeling was assessed by morphologic analysis. We found that the angiotensin II-induced increase in diastolic pressure was significantly higher in iPLA(2)β-Tg than iPLA(2)β-Wt mice, whereas, the basal blood pressure was not significantly different. The media thickness and media∶lumen ratio of the mesenteric arteries were significantly increased in angiotensin II-infused iPLA(2)β-Tg mice. Analysis revealed no difference in vascular smooth muscle cell proliferation. In contrast, adenovirus-mediated iPLA(2)β overexpression in cultured vascular smooth muscle cells promoted angiotensin II-induced [(3)H]-leucine incorporation, indicating enhanced hypertrophy. Moreover, angiotensin II infusion-induced c-Jun phosphorylation in vascular smooth muscle cells overexpressing iPLA2β to higher levels, which was abolished by inhibition of 12/15 lipoxygenase. In addition, we found that angiotensin II up-regulated the endogenous iPLA(2)β protein in-vitro and in-vivo.The present study reports that iPLA(2)β up-regulation exacerbates angiotensin II-induced vascular smooth muscle cell hypertrophy, vascular remodeling and hypertension via the 12/15 lipoxygenase and c-Jun pathways.http://europepmc.org/articles/PMC3282780?pdf=render
spellingShingle Lindsay E Calderon
Shu Liu
Wen Su
Zhongwen Xie
Zhenheng Guo
Wanda Eberhard
Ming C Gong
iPLA2β overexpression in smooth muscle exacerbates angiotensin II-induced hypertension and vascular remodeling.
PLoS ONE
title iPLA2β overexpression in smooth muscle exacerbates angiotensin II-induced hypertension and vascular remodeling.
title_full iPLA2β overexpression in smooth muscle exacerbates angiotensin II-induced hypertension and vascular remodeling.
title_fullStr iPLA2β overexpression in smooth muscle exacerbates angiotensin II-induced hypertension and vascular remodeling.
title_full_unstemmed iPLA2β overexpression in smooth muscle exacerbates angiotensin II-induced hypertension and vascular remodeling.
title_short iPLA2β overexpression in smooth muscle exacerbates angiotensin II-induced hypertension and vascular remodeling.
title_sort ipla2β overexpression in smooth muscle exacerbates angiotensin ii induced hypertension and vascular remodeling
url http://europepmc.org/articles/PMC3282780?pdf=render
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