Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-7-21
pubmed:abstractText
The renin-angiotensin system plays an important role in the hypertrophic responses in cardiac myocytes through the activation of signal transduction pathways and expression of oncogenes. In the present study, we examined mechanical stretch-induced activation of mitogen-activated protein kinases (MAP kinases) using cultured cardiac myocytes derived from neonatal angiotensinogen gene deficient mice (Agt-/-) and neonatal wild type mice (Agt+/+). Within 2 minutes of being added to cardiac myocytes, angiotensin II activated MAP kinases and the response was completely blocked by pretreatment of the cardiac myocytes with CV-11974, a selective antagonist of angiotensin II type 1 receptors. Interestingly, mechanical stretch resulted in significantly greater activation of MAP kinases in Agt-/- cardiac myocytes than in Agt+/+ cardiac myocytes. CV-11974 failed to suppress the stretch-induced activation of MAP kinases in Agt-/- cardiac myocytes while it inhibited the activation in Agt+/+ cardiac myocytes. BQ123, an endothelin type A receptor antagonist, had no effect on stretch-induced activation of MAP kinases in cardiac myocytes from either mouse strain. These results suggest that cardiac RAS is important for stretch-induced MAP kinase activation in Agt+/+ cardiac myocytes; however, angiotensin II is not indispensable for mechanical stretch-induced activation of MAP kinases in Agt-/- cardiac myocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II, http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin Receptor Antagonists, http://linkedlifedata.com/resource/pubmed/chemical/Angiotensinogen, http://linkedlifedata.com/resource/pubmed/chemical/Benzimidazoles, http://linkedlifedata.com/resource/pubmed/chemical/Calcium-Calmodulin-Dependent..., http://linkedlifedata.com/resource/pubmed/chemical/Endothelin-1, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 1, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 3, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Peptides, Cyclic, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Endothelin, http://linkedlifedata.com/resource/pubmed/chemical/Tetrazoles, http://linkedlifedata.com/resource/pubmed/chemical/candesartan, http://linkedlifedata.com/resource/pubmed/chemical/cyclo(Trp-Asp-Pro-Val-Leu)
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
9
pubmed:volume
235
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
36-41
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:9196031-Angiotensin II, pubmed-meshheading:9196031-Angiotensin Receptor Antagonists, pubmed-meshheading:9196031-Angiotensinogen, pubmed-meshheading:9196031-Animals, pubmed-meshheading:9196031-Benzimidazoles, pubmed-meshheading:9196031-Blotting, Western, pubmed-meshheading:9196031-Calcium-Calmodulin-Dependent Protein Kinases, pubmed-meshheading:9196031-Cells, Cultured, pubmed-meshheading:9196031-Endothelin-1, pubmed-meshheading:9196031-Enzyme Activation, pubmed-meshheading:9196031-Gene Targeting, pubmed-meshheading:9196031-Mice, pubmed-meshheading:9196031-Mice, Transgenic, pubmed-meshheading:9196031-Mitogen-Activated Protein Kinase 1, pubmed-meshheading:9196031-Mitogen-Activated Protein Kinase 3, pubmed-meshheading:9196031-Mitogen-Activated Protein Kinases, pubmed-meshheading:9196031-Myocardium, pubmed-meshheading:9196031-Peptides, Cyclic, pubmed-meshheading:9196031-Receptors, Endothelin, pubmed-meshheading:9196031-Renin-Angiotensin System, pubmed-meshheading:9196031-Tetrazoles
pubmed:year
1997
pubmed:articleTitle
Stretch-induced MAP kinase activation in cardiomyocytes of angiotensinogen-deficient mice.
pubmed:affiliation
Second Department of Internal Medicine, Yokohama City University School of Medicine, Yokohama, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't