Linked Life Data

18314486

Source:http://linkedlifedata.com/resource/pubmed/id/18314486

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-3-3
pubmed:abstractText
Angiotensin II has been shown to be a cytokine especially acting as a growth factor. A local renin-angiotensin system has been identified in the prostate gland, and the physiologic function of angiotensin II seems to be similar in prostate cancer, as we previously reported. In the present study, we explored the biological role of angiotensin II in oxidative stress of prostate cancer cells. Activated Akt was determined, and the expression of oxidative stress-related proteins (p47phox, manganese superoxide dismutase 2, glutathione peroxidase) was examined by Western blotting in LNCaP cells, which were stimulated with angiotensin II and/or an angiotensin II receptor type 1 blocker, candesartan. To examine DNA damage induced by angiotensin II, 8-hydroxy-2'-deoxyguanosine was determined, and Western blots were analyzed to detect checkpoint proteins including p53, Chk2, and cdc2. Immunocytochemical studies of inducible nitric oxide synthase and superoxide anion radical (O(2)(-)) were done in LNCaP cells stimulated with angiotensin II. The phosphorylation of Akt was induced by angiotensin II treatment and inhibited by candesartan, as well as by LY294002, an inhibitor of phosphoinositide 3-kinase. Oxidative stress-related proteins were up-regulated by angiotensin II and inhibited by pretreatment with candesartan or catalase. The level of 8-hydroxy-2'-deoxyguanosine was increased by angiotensin II and conversely decreased by candesartan. Immunocytochemical studies showed that angiotensin II enhanced an inflammatory marker, inducible nitric oxide synthase, and the production of O(2)(-) radical. The hypothesis that angiotensin II has the potential to induce oxidative stress, which may be implicated in carcinogenesis of the prostate gland through long-term exposure to chronic inflammation is proposed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1541-7786
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
250-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:18314486-Angiotensin II, pubmed-meshheading:18314486-Angiotensin II Type 1 Receptor Blockers, pubmed-meshheading:18314486-Cell Cycle Proteins, pubmed-meshheading:18314486-Cell Line, Tumor, pubmed-meshheading:18314486-DNA Damage, pubmed-meshheading:18314486-Deoxyguanosine, pubmed-meshheading:18314486-Humans, pubmed-meshheading:18314486-Immunohistochemistry, pubmed-meshheading:18314486-Male, pubmed-meshheading:18314486-Microscopy, Confocal, pubmed-meshheading:18314486-Models, Biological, pubmed-meshheading:18314486-Nitric Oxide Synthase Type II, pubmed-meshheading:18314486-Oxidative Stress, pubmed-meshheading:18314486-Phosphorylation, pubmed-meshheading:18314486-Prostatic Neoplasms, pubmed-meshheading:18314486-Proto-Oncogene Proteins c-akt, pubmed-meshheading:18314486-Receptor, Angiotensin, Type 1, pubmed-meshheading:18314486-Superoxides, pubmed-meshheading:18314486-Time Factors
pubmed:year
2008
pubmed:articleTitle
Angiotensin II induces oxidative stress in prostate cancer.
pubmed:affiliation
Department of Urology, Yokohama City University School of Medicine, Yokohama, Japan. hu0428@med.yokohama-cu.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't