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CREB Downregulation in Vascular Disease A Common Response to Cardiovascular Risk

CREB Downregulation in Vascular Disease A Common Response to Cardiovascular Risk CREB Downregulation in Vascular Disease A Common Response to Cardiovascular Risk Irene E. Schauer, Leslie A. Knaub, Monique Lloyd, Peter A. Watson, Catherine Gliwa, Katherine E. Lewis, Alan Chait, Dwight J. Klemm, Jody M. Gunter, Ron Bouchard, Thomas O. McDonald, Kevin D. O’Brien, Jane E.B. Reusch Objective—To examine the impact of low-density lipoprotein (LDL), an established mediator of atherosclerosis, on the transcription factor cAMP-response element-binding protein (CREB), which is a regulator of vascular smooth muscle cell (VSMC) quiescence. Methods and Results—VSMC CREB content is diminished in rodent models of diabetes and pulmonary hypertension. We examined aortic CREB content in rodent models of aging, hypertension, and insulin resistance, and we determined nuclear CREB protein in the medial VSMC of high-fat-fed LDL receptor-null mice. There was significant loss of CREB protein in all models. In vitro, primary culture rat aortic VSMC exposed to LDL and oxidized LDL exhibited a rapid, transient increase in CREB phosphorylation and transient phosphorylation/activation of Akt, ERK, JNK, ans p38 MAPK. Exposure to oxidized LDL, but not to LDL, for 24 to 48 hours decreased CREB protein in a dose-dependent fashion and led to nuclear exclusion of CREB. Pharmacological reactive oxygen species scavengers and inhibition of ERK http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis, Thrombosis, and Vascular Biology Wolters Kluwer Health

CREB Downregulation in Vascular Disease A Common Response to Cardiovascular Risk

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/lp/wolters-kluwer-health/creb-downregulation-in-vascular-disease-a-common-response-to-8lewEka5RL
ISSN
1079-5642
eISSN
1524-4636
DOI
10.1161/ATVBAHA.109.199133
pmid
20150559

Abstract

CREB Downregulation in Vascular Disease A Common Response to Cardiovascular Risk Irene E. Schauer, Leslie A. Knaub, Monique Lloyd, Peter A. Watson, Catherine Gliwa, Katherine E. Lewis, Alan Chait, Dwight J. Klemm, Jody M. Gunter, Ron Bouchard, Thomas O. McDonald, Kevin D. O’Brien, Jane E.B. Reusch Objective—To examine the impact of low-density lipoprotein (LDL), an established mediator of atherosclerosis, on the transcription factor cAMP-response element-binding protein (CREB), which is a regulator of vascular smooth muscle cell (VSMC) quiescence. Methods and Results—VSMC CREB content is diminished in rodent models of diabetes and pulmonary hypertension. We examined aortic CREB content in rodent models of aging, hypertension, and insulin resistance, and we determined nuclear CREB protein in the medial VSMC of high-fat-fed LDL receptor-null mice. There was significant loss of CREB protein in all models. In vitro, primary culture rat aortic VSMC exposed to LDL and oxidized LDL exhibited a rapid, transient increase in CREB phosphorylation and transient phosphorylation/activation of Akt, ERK, JNK, ans p38 MAPK. Exposure to oxidized LDL, but not to LDL, for 24 to 48 hours decreased CREB protein in a dose-dependent fashion and led to nuclear exclusion of CREB. Pharmacological reactive oxygen species scavengers and inhibition of ERK

Journal

Arteriosclerosis, Thrombosis, and Vascular BiologyWolters Kluwer Health

Published: Apr 1, 2010

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