Linked Life Data

8041116

Source:http://linkedlifedata.com/resource/pubmed/id/8041116

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1994-8-19
pubmed:abstractText
A single intravenous injection of lead nitrate to rats induces a synchronized wave of hepatocyte proliferation without accompanying liver cell necrosis. However, the mechanism of the mitogenic effect of lead nitrate is not known, and whether hepatocyte growth factor (HGF), transforming growth factor-alpha (TGF-alpha), and transforming growth factor-beta 1 (TGF-beta 1) play any role in it have not been investigated. These growth factors have indeed been shown to provide either positive or negative stimuli for liver cell regeneration after partial hepatectomy or liver cell necrosis. Moreover, there are reports showing that administration of non-necrogenic doses of tumor necrosis factor-alpha (TNF-alpha) to rats lead to an enhanced proliferation of hepatocytes and liver nonparenchymal cells. Lead is known to sensitize animals to lethal effects of bacterial lipopolysaccharides (LPS), suggesting that lead nitrate may modify the production of TNF-alpha in response to endogenous LPS of intestinal origin. An enhanced production of TNF-alpha could therefore be involved in the mitogenic action of lead nitrate.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0023-6837
pubmed:author
pubmed:issnType
Print
pubmed:volume
71
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
35-41
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Roles of growth factors and of tumor necrosis factor-alpha on liver cell proliferation induced in rats by lead nitrate.
pubmed:affiliation
Department of Pathology, University of Pittsburgh School of Medicine, Pennsylvania.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't