Source:http://linkedlifedata.com/resource/pubmed/id/11162525
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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0018284,
umls-concept:C0021469,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0079183,
umls-concept:C0087111,
umls-concept:C0227525,
umls-concept:C0442796,
umls-concept:C0521115,
umls-concept:C0598312,
umls-concept:C0752312,
umls-concept:C1280500,
umls-concept:C1370600,
umls-concept:C1704259,
umls-concept:C1705987
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pubmed:issue |
1
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pubmed:dateCreated |
2001-2-22
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pubmed:abstractText |
Several growth factors play an important role in liver regeneration. Once hepatic injury occurs, liver regeneration is stimulated by hepatocyte growth factor (HGF), transforming growth factor (TGF)-alpha, and heparin-binding epidermal growth factor-like growth factor (HB-EGF), whereas TGF-beta1 terminates liver regeneration. In this study, we analyzed the effect of a combination of HGF and epidermal growth factor (EGF) on mitogen-activated protein kinase (MAPK) activity and G1 cyclin expression in primary cultured rat hepatocytes. Treatment with a combination of HGF and EGF, in comparison with that of either HGF or EGF, induced tyrosine phosphorylation of both c-Met and EGF receptor (EGFR) independently and additively stimulated MAPK activity and cyclin D1 expression, resulting in additive stimulation of DNA synthesis. On the other hand, although TGF-beta1 treatment did not affect tyrosine phosphorylation of c-Met and EGFR, MAPK activity, and cyclin D1 expression, which were stimulated by HGF and EGF, DNA synthesis was completely inhibited through a marked decrease in cyclin E expression. These results indicate that potent mitogens, such as HGF, TGF-alpha, and HB-EGF, could induce the additive enhancement of liver regeneration cooperatively through an increase in Ras/MAPK activity followed by cyclin D1 expression, and that TGF-beta1 suppresses the growth factor-induced signals between cyclin D1 and cyclin E, resulting in the inhibition of DNA synthesis.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin D1,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/Epidermal Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Substances,
http://linkedlifedata.com/resource/pubmed/chemical/Hepatocyte Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0006-291X
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2001 Academic Press.
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pubmed:issnType |
Print
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pubmed:day |
12
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pubmed:volume |
280
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
368-73
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:11162525-Animals,
pubmed-meshheading:11162525-Cells, Cultured,
pubmed-meshheading:11162525-Cyclin D1,
pubmed-meshheading:11162525-DNA,
pubmed-meshheading:11162525-Epidermal Growth Factor,
pubmed-meshheading:11162525-G1 Phase,
pubmed-meshheading:11162525-Growth Substances,
pubmed-meshheading:11162525-Hepatocyte Growth Factor,
pubmed-meshheading:11162525-Hepatocytes,
pubmed-meshheading:11162525-Kinetics,
pubmed-meshheading:11162525-Liver,
pubmed-meshheading:11162525-MAP Kinase Signaling System,
pubmed-meshheading:11162525-Male,
pubmed-meshheading:11162525-Mitogen-Activated Protein Kinases,
pubmed-meshheading:11162525-Rats,
pubmed-meshheading:11162525-Rats, Wistar,
pubmed-meshheading:11162525-Transforming Growth Factor beta
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pubmed:year |
2001
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pubmed:articleTitle |
Additive and inhibitory effects of simultaneous treatment with growth factors on DNA synthesis through MAPK pathway and G1 cyclins in rat hepatocytes.
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pubmed:affiliation |
Department of Internal Medicine II, Miyazaki Medical College, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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