Linked Life Data

12801513

Source:http://linkedlifedata.com/resource/pubmed/id/12801513

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2003-6-12
pubmed:abstractText
Angiotensin II (AT II) is thought to be associated with the development of renal interstitial fibrosis. However, the molecular mechanisms of the interstitial fibrosis have not been extensively studied. We have examined the role of mitogen-activated protein kinases (MAPKs) on fibronectin (FN) accumulation in cultured normal rat kidney interstitial fibroblasts (NRK 49F cell line). AT II caused dose-dependent increases in FN accumulation and FN mRNA in these cells. AT II also activated the extracellular signal-regulated kinase (ERK) and p38 MAPK in the presence of AT II. These increases in FN accumulation and activation of MAPKs were inhibited with AT I receptor antagonist (ARB; CV-11974) in renal interstitial fibroblasts. The inhibitors against ERK (PD98059) and p38 MAPK (SB203580) significantly inhibited AT II-induced increases in FN mRNA. These findings suggest that the MAPKs play an important role in AT II-mediated renal interstitial fibrosis and that ARB may be useful for preventing renal interstitial fibrosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0003-9861
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
415
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
63-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Possible involvement of mitogen-activated protein kinase in the angiotensin II-induced fibronectin synthesis in renal interstitial fibroblasts.
pubmed:affiliation
Department of Medicine, Kidney Center, Tokyo Women's Medical University, Tokyo 162-8666, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't