Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2002-9-20
pubmed:abstractText
The pharmacological interaction between pepstatin A, a specific inhibitor of cathepsin D, and N-acetyl-L-cysteine was analyzed using hepatic stellate cells in primary culture. Isolated rat stellate cells were cultured on plastic dishes in Dulbecco's modified Eagle's medium (DMEM). Proteins and phospho-proteins were detected by Western blot. DNA synthesis was determined by [3H]thymidine uptake. Pepstatin A restored DNA synthesis of stellate cells stimulated by either platelet-derived growth factor-BB (PDGF-BB) or insulin-like growth factor-I (IGF-I), an effect that was attenuated by N-acetyl-L-cysteine. This agent induced the recovery of both the expression of PDGF receptor beta and IGF-I receptor beta and the phosphorylation of p42/44 mitogen-activated protein kinase (MAPK) and Akt under stimulation with either PDGF-BB or IGF-I, which were downregulated by N-acetyl-L-cysteine. Expression of cathepsin D was induced in activated stellate cells. These results indicate that pepstatin A hampers the inhibitory effect of N-acetyl-L-cysteine on stellate cell growth by ameliorating growth factor receptor downregulation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0014-2999
pubmed:author
pubmed:copyrightInfo
Copyright 2002 Elsevier Science B.V.
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
451
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
265-70
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Pepstatin A attenuates the inhibitory effect of N-acetyl-L-cysteine on proliferation of hepatic myofibroblasts (stellate cells).
pubmed:affiliation
Department of Hepatology, Graduate School of Medicine, Osaka City University, 1-4-3 Asahimachi, Abeno 545-8585 Osaka, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't