Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2003-11-17
pubmed:abstractText
Angiotensin II contributes to ventricular remodeling by promoting both cardiac hypertrophy and apoptosis; however, the mechanism underlying the latter phenomenon is poorly understood. One possibility that has been advanced is that angiotensin II activates NADPH oxidase, generating free radicals that trigger apoptosis. In apparent support of this notion, it was found that angiotensin II-mediated apoptosis in the cardiomyocyte is blocked by the NADPH oxidase inhibitor diphenylene iodonium. However, three lines of evidence suggest that peroxynitrite, rather than superoxide, is responsible for angiotensin II-mediated DNA damage and apoptosis. First, the inducible nitric oxide inhibitor aminoguanidine prevents angiotensin II-induced DNA damage and apoptosis. Second, based on ligation-mediated PCR, the pattern of angiotensin II-induced DNA damage resembles peroxynitritemediated damage rather than damage caused by either superoxide or nitric oxide. Third, angiotensin II activates p53 through the phosphorylation of Ser15 and Ser20, residues that are commonly phosphorylated in response to DNA damage. It is proposed that angiotensin II promotes the oxidation of DNA, which in turn activates p53 to mediate apoptosis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II, http://linkedlifedata.com/resource/pubmed/chemical/Casp9 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Caspase 9, http://linkedlifedata.com/resource/pubmed/chemical/Caspases, http://linkedlifedata.com/resource/pubmed/chemical/DNA, Mitochondrial, http://linkedlifedata.com/resource/pubmed/chemical/Free Radicals, http://linkedlifedata.com/resource/pubmed/chemical/NADPH Oxidase, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II, http://linkedlifedata.com/resource/pubmed/chemical/Nos2 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2, http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Protein p53, http://linkedlifedata.com/resource/pubmed/chemical/Vasoconstrictor Agents, http://linkedlifedata.com/resource/pubmed/chemical/bcl-2-Associated X Protein
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
285
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H2364-72
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:12919932-Angiotensin II, pubmed-meshheading:12919932-Animals, pubmed-meshheading:12919932-Animals, Newborn, pubmed-meshheading:12919932-Apoptosis, pubmed-meshheading:12919932-Base Sequence, pubmed-meshheading:12919932-Caspase 9, pubmed-meshheading:12919932-Caspases, pubmed-meshheading:12919932-Cells, Cultured, pubmed-meshheading:12919932-DNA, Mitochondrial, pubmed-meshheading:12919932-DNA Damage, pubmed-meshheading:12919932-Free Radicals, pubmed-meshheading:12919932-Myocytes, Cardiac, pubmed-meshheading:12919932-NADPH Oxidase, pubmed-meshheading:12919932-Nitric Oxide Synthase, pubmed-meshheading:12919932-Nitric Oxide Synthase Type II, pubmed-meshheading:12919932-Protein Kinase C, pubmed-meshheading:12919932-Proto-Oncogene Proteins, pubmed-meshheading:12919932-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:12919932-Rats, pubmed-meshheading:12919932-Signal Transduction, pubmed-meshheading:12919932-Tumor Suppressor Protein p53, pubmed-meshheading:12919932-Vasoconstrictor Agents, pubmed-meshheading:12919932-bcl-2-Associated X Protein
pubmed:year
2003
pubmed:articleTitle
Apoptotic cascade initiated by angiotensin II in neonatal cardiomyocytes: role of DNA damage.
pubmed:affiliation
Department of Pharmacology, University of South Alabama School of Medicine, Mobile, AL 36688, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.