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Title: Regulation of ERK5 by insulin and angiotensin-II in vascular smooth muscle cells

Abstract

ERK5 is involved in proliferation of vascular smooth muscle cells (VSMC). The proliferative actions of insulin and angiotensin-II (A-II) in VSMC are mediated in part by ERK1/2. We hypothesized that insulin and A-II also regulate ERK5 activity in VSMC. Acute treatment (<60 min) with insulin or A-II increased phosphorylation of ERK1/2 at 15 min and ERK5 at 5 min. Chronic treatment ({<=}8 h) with insulin increased ERK1/2 phosphorylation by 4 h and ERK5 by 8 h. A-II-stimulated phosphorylation of ERK1/2 by 8 h and ERK5 by 4 h. The EC{sub 50} for insulin treatment effecting ERK1/2 and ERK5 phosphorylation was 1.5 and 0.1 nM, whereas the EC{sub 50} for A-II was 2 nM, each. Insulin plus A-II induced an additive effect only on ERK5 phosphorylation. Inhibition of insulin- and A-II-stimulated phosphorylation of ERK5 and ERK1/2 by PD98059 and Wortmannin exhibited differential and time-dependent effects. Taken together, these data indicate that insulin and A-II regulate the activity of ERK5, but different from that seen for ERK1/2.

Authors:
 [1];  [1];  [2];
  1. University of Colorado at Denver and Health Sciences Center, Aurora, CO (United States)
  2. (United States)
Publication Date:
OSTI Identifier:
20979848
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 354; Journal Issue: 4; Other Information: DOI: 10.1016/j.bbrc.2007.01.102; PII: S0006-291X(07)00163-5; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ADDITIVES; ANGIOTENSIN; BIOLOGICAL STRESS; CELL PROLIFERATION; GENE REGULATION; INHIBITION; INSULIN; MUSCLES; PHOSPHORYLATION; TIME DEPENDENCE

Citation Formats

Sharma, Girish, Goalstone, Marc Lee, Veterans Affairs Medical Center, Denver, CO 80220, and E-mail: Marc.Goalstone@uchsc.edu. Regulation of ERK5 by insulin and angiotensin-II in vascular smooth muscle cells. United States: N. p., 2007. Web. doi:10.1016/j.bbrc.2007.01.102.
Sharma, Girish, Goalstone, Marc Lee, Veterans Affairs Medical Center, Denver, CO 80220, & E-mail: Marc.Goalstone@uchsc.edu. Regulation of ERK5 by insulin and angiotensin-II in vascular smooth muscle cells. United States. doi:10.1016/j.bbrc.2007.01.102.
Sharma, Girish, Goalstone, Marc Lee, Veterans Affairs Medical Center, Denver, CO 80220, and E-mail: Marc.Goalstone@uchsc.edu. Fri . "Regulation of ERK5 by insulin and angiotensin-II in vascular smooth muscle cells". United States. doi:10.1016/j.bbrc.2007.01.102.
@article{osti_20979848,
title = {Regulation of ERK5 by insulin and angiotensin-II in vascular smooth muscle cells},
author = {Sharma, Girish and Goalstone, Marc Lee and Veterans Affairs Medical Center, Denver, CO 80220 and E-mail: Marc.Goalstone@uchsc.edu},
abstractNote = {ERK5 is involved in proliferation of vascular smooth muscle cells (VSMC). The proliferative actions of insulin and angiotensin-II (A-II) in VSMC are mediated in part by ERK1/2. We hypothesized that insulin and A-II also regulate ERK5 activity in VSMC. Acute treatment (<60 min) with insulin or A-II increased phosphorylation of ERK1/2 at 15 min and ERK5 at 5 min. Chronic treatment ({<=}8 h) with insulin increased ERK1/2 phosphorylation by 4 h and ERK5 by 8 h. A-II-stimulated phosphorylation of ERK1/2 by 8 h and ERK5 by 4 h. The EC{sub 50} for insulin treatment effecting ERK1/2 and ERK5 phosphorylation was 1.5 and 0.1 nM, whereas the EC{sub 50} for A-II was 2 nM, each. Insulin plus A-II induced an additive effect only on ERK5 phosphorylation. Inhibition of insulin- and A-II-stimulated phosphorylation of ERK5 and ERK1/2 by PD98059 and Wortmannin exhibited differential and time-dependent effects. Taken together, these data indicate that insulin and A-II regulate the activity of ERK5, but different from that seen for ERK1/2.},
doi = {10.1016/j.bbrc.2007.01.102},
journal = {Biochemical and Biophysical Research Communications},
number = 4,
volume = 354,
place = {United States},
year = {Fri Mar 23 00:00:00 EDT 2007},
month = {Fri Mar 23 00:00:00 EDT 2007}
}