Linked Life Data

8125929

Source:http://linkedlifedata.com/resource/pubmed/id/8125929

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1994-4-12
pubmed:abstractText
Angiotensin II has been shown to induce hypertrophy of cultured vascular smooth muscle cells (VSMC). To understand the mechanisms of induction of the hypertrophy, we studied its effect on the phosphorylation state of eIF-4E, a rate-limiting eukaryotic protein synthesis initiation factor whose activity has been shown to be regulated by phosphorylation. Angiotensin II induced a 2-3-fold increase in the phosphorylation of eIF-4E in VSMC. The stimulation of phosphorylation was apparent at 20 min and persisted for at least 12 h. Phosphoamino acid analysis revealed that serine is the major residue of eIF-4E phosphorylated by angiotensin II. Staurosporine and calphostin C, two potent inhibitors of the serine/threonine protein kinase, protein kinase C, significantly attenuated the angiotensin II-induced eIF-4E phosphorylation. Staurosporine and calphostin C also blunted the angiotensin II-stimulated protein synthesis. Together, these observations indicate that angiotensin II induces phosphorylation of eIF-4E in a protein kinase C-dependent manner and suggest that this pathway may play an important role in the mechanism by which angiotensin II causes hypertrophy of VSMC.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
11
pubmed:volume
269
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7180-4
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Angiotensin II induces phosphorylation of eukaryotic protein synthesis initiation factor 4E in vascular smooth muscle cells.
pubmed:affiliation
Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia 30322.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't