Source:http://linkedlifedata.com/resource/pubmed/id/16024575
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2005-11-14
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pubmed:abstractText |
ANG-(1-7) improves the function of the remodeling heart. Although this peptide is generated directly within the myocardium, the effects of ANG-(1-7) on cardiac fibroblasts that play a critical role in cardiac remodeling are largely unknown. We tested the hypothesis that specific binding of ANG-(1-7) to cardiac fibroblasts regulates cellular functions that are involved in cardiac remodeling. 125I-labeled ANG-(1-7) binding assays identified specific binding sites of ANG-(1-7) on adult rat cardiac fibroblasts (ARCFs) with an affinity of 11.3 nM and a density of 131 fmol/mg protein. At nanomolar concentrations, ANG-(1-7) interacted with specific sites that were distinct from ANG II type 1 and type 2 receptors without increasing cytosolic Ca2+ concentration. At these concentrations, ANG-(1-7) had inhibitory effects on collagen synthesis as assessed by [3H]proline incorporation and decreased mRNA expression of growth factors in ARCFs. These effects of ANG-(1-7) contrasted with effects of ANG II. Pretreatment of ARCFs with ANG-(1-7) inhibited ANG II-induced increases in collagen synthesis and in mRNA expression of growth factors, including endothelin-1 and leukemia inhibitory factor. ANG-(1-7) pretreatment also inhibited the stimulatory effects of conditioned medium from ANG II-treated ARCFs on [3H]leucine incorporation and atrial natriuretic factor mRNA expression, markers of hypertrophy, in cardiomyocytes. Thus ANG-(1-7) interacted with specific receptors on ARCFs to exert potential antifibrotic and antitrophic effects that could reverse ANG II effects. These results suggest that ANG-(1-7) may play an important role in the heart in regulating cardiac remodeling.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin I,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Collagen,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Substances,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/angiotensin I (1-7)
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0363-6135
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
289
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H2356-63
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:16024575-Angiotensin I,
pubmed-meshheading:16024575-Animals,
pubmed-meshheading:16024575-Binding Sites,
pubmed-meshheading:16024575-Calcium,
pubmed-meshheading:16024575-Cells, Cultured,
pubmed-meshheading:16024575-Collagen,
pubmed-meshheading:16024575-Dose-Response Relationship, Drug,
pubmed-meshheading:16024575-Fibroblasts,
pubmed-meshheading:16024575-Fibrosis,
pubmed-meshheading:16024575-Growth Substances,
pubmed-meshheading:16024575-Heart Ventricles,
pubmed-meshheading:16024575-Male,
pubmed-meshheading:16024575-Peptide Fragments,
pubmed-meshheading:16024575-Protein Binding,
pubmed-meshheading:16024575-Rats,
pubmed-meshheading:16024575-Rats, Sprague-Dawley
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pubmed:year |
2005
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pubmed:articleTitle |
Angiotensin-(1-7) binds to specific receptors on cardiac fibroblasts to initiate antifibrotic and antitrophic effects.
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pubmed:affiliation |
Dept. of Medicine/Cardiology, UCSD Medical Center, 200 West Arbor Dr., San Diego, CA 92103-8411, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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