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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1994-8-22
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pubmed:abstractText |
Inhibitors of the production of endogenous angiotensin II (A-II) can diminish the hyperplastic response produced by arterial injury in animals; however, a similar effect in humans has not been observed. To explain this discrepancy, we compared the effect of A-II on rat aortic smooth muscle cells (R-SMC) and smooth muscle cells derived from human saphenous veins (H-SMC). A-II (10-1000 nM) significantly increased the proliferative rate of R-SMC incubated in 10% serum, but a similar effect was not observed with H-SMC. Incubation of R-SMC for 24 hr with A-II (1 microM) produced a significant increase in cell size (7%) and protein production (18%), whereas no hypertrophic response was noted in H-SMC exposed to A-II. In neither R-SMC nor H-SMC did A-II, in any concentration, induce cell migration. Stimulation of R-SMC with A-II resulted in tyrosine phosphorylation of five proteins (approximately 120, approximately 108, approximately 68, 45, 42 kDa). The 42- and 45-kDa proteins, which we have previously identified as mitogen-activated protein kinases (MAP-K), remained phosphorylated for 1 hr. In H-SMC, only MAP kinases were tyrosine phosphorylated, but with less intensity than in R-SMC, and only for 20 min. In protein kinase C-depleted SMC, tyrosine phosphorylation of MAP kinase was inhibited in both cell types. A-II produced hypertrophy and hyperplasia of R-SMC, but not H-SMC. Differences in intracellular signaling might account for these disparate effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0022-4804
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
57
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
174-8
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:8041134-Angiotensin II,
pubmed-meshheading:8041134-Animals,
pubmed-meshheading:8041134-Calcium-Calmodulin-Dependent Protein Kinases,
pubmed-meshheading:8041134-Cell Division,
pubmed-meshheading:8041134-Humans,
pubmed-meshheading:8041134-Hypertrophy,
pubmed-meshheading:8041134-Muscle, Smooth, Vascular,
pubmed-meshheading:8041134-Phosphorylation,
pubmed-meshheading:8041134-Rats,
pubmed-meshheading:8041134-Rats, Sprague-Dawley,
pubmed-meshheading:8041134-Species Specificity,
pubmed-meshheading:8041134-Tyrosine
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pubmed:year |
1994
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pubmed:articleTitle |
Effect of angiotensin II on human vascular smooth muscle cell growth.
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pubmed:affiliation |
Department of Surgery, Beth Israel Hospital, Boston, Massachusetts 02215.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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