Source:http://linkedlifedata.com/resource/pubmed/id/12444203
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| Predicate | Object |
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| rdf:type | |
| lifeskim:mentions | |
| pubmed:dateCreated |
2002-11-21
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| pubmed:abstractText |
It has been recently shown that in ischemic rat kidneys activin A is induced in tubular cells and inhibits their regeneration. The present study was conducted to further investigate the action of activin A in tubular cells during regeneration. Among genes thought to be critical for kidney development, Pax-2 was upregulated in tubular cells during regeneration after renal ischemia. Pax-2 protein was localized in nuclei of tubular and interstitial cells, some of which co-expressed a mesenchymal cell marker, vimentin, suggesting that a population of Pax-2-positive cells have properties of immature progenitor-like tubular cells. The Pax-2-expressing cells co-expressed a cell proliferation marker, BrdU, activin A, and the type II activin receptor. Activin A modulated growth of BrdU/Pax-2 double-positive cells since an administration of follistatin increased; conversely, exogenous activin A decreased the number of BrdU/Pax-2 double-positive cells after renal ischemia. Activin A also reduced the expression of Pax-2 in cultured metanephroi. A proximal tubular cell line, LLC-PK(1) cells, was used to further study the mode of action of activin A. The expression of Pax-2 was not detected in quiescent LLC-PK(1) cells, but it was markedly increased when growth was stimulated. Under this condition, activin A significantly inhibited DNA synthesis and reduced the expression of Pax-2 in LLC-PK(1) cells. In contrast, blockade of the activin signaling by overexpressing dominantly negative mutant receptor enhanced the expression level of Pax-2 in LLC-PK(1) cells and induced an immature phenotype. These results suggest that activin A regulates tubular cell growth and differentiation by modulating the expression of Pax-2 during regeneration.
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| pubmed:language |
eng
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| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Activin Receptors, Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Activins,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Follistatin,
http://linkedlifedata.com/resource/pubmed/chemical/Inhibin-beta Subunits,
http://linkedlifedata.com/resource/pubmed/chemical/PAX2 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/PAX2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Vimentin,
http://linkedlifedata.com/resource/pubmed/chemical/activin A
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| pubmed:status |
MEDLINE
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| pubmed:author | |
| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
2850-9
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| pubmed:dateRevised |
2009-11-19
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| pubmed:articleTitle |
Involvement of Pax-2 in the action of activin A on tubular cell regeneration.
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| pubmed:affiliation |
Institute for Molecular and Cellular Regulation, Gunma University, Maebashi 371-8512, Japan.
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