pubmed-article:18047832 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18047832 | lifeskim:mentions | umls-concept:C0015576 | lld:lifeskim |
pubmed-article:18047832 | lifeskim:mentions | umls-concept:C0870134 | lld:lifeskim |
pubmed-article:18047832 | lifeskim:mentions | umls-concept:C0225828 | lld:lifeskim |
pubmed-article:18047832 | lifeskim:mentions | umls-concept:C0521324 | lld:lifeskim |
pubmed-article:18047832 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
pubmed-article:18047832 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
pubmed-article:18047832 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:18047832 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:18047832 | pubmed:dateCreated | 2007-12-17 | lld:pubmed |
pubmed-article:18047832 | pubmed:abstractText | The existence of skeletal muscle-derived stem cells (MDSCs) has been suggested in mammals; however, the signaling pathways controlling MDSC proliferation remain largely unknown. Here we report the isolation of myosphere-derived progenitor cells (MDPCs) that can give rise to beating cardiomyocytes from adult skeletal muscle. We identified that follistatin, an antagonist of TGF-beta family members, was predominantly expressed in MDPCs, whereas myostatin was mainly expressed in myogenic cells and mature skeletal muscle. Although follistatin enhanced the replicative growth of MDPCs through Smad2/3 inactivation and cell cycle progression, disruption of myostatin did not increase the MDPC proliferation. By contrast, inhibition of activin A (ActA) or growth differentiation factor 11 (GDF11) signaling dramatically increased MDPC proliferation via down-regulation of p21 and increases in the levels of cdk2/4 and cyclin D1. Thus, follistatin may be an effective progenitor-enhancing agent neutralizing ActA and GDF11 signaling to regulate the growth of MDPCs in skeletal muscle. | lld:pubmed |
pubmed-article:18047832 | pubmed:language | eng | lld:pubmed |
pubmed-article:18047832 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18047832 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:18047832 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18047832 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18047832 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18047832 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18047832 | pubmed:month | Jan | lld:pubmed |
pubmed-article:18047832 | pubmed:issn | 1090-2104 | lld:pubmed |
pubmed-article:18047832 | pubmed:author | pubmed-author:TakahashiTomo... | lld:pubmed |
pubmed-article:18047832 | pubmed:author | pubmed-author:MatsubaraHiro... | lld:pubmed |
pubmed-article:18047832 | pubmed:author | pubmed-author:AshiharaEishi... | lld:pubmed |
pubmed-article:18047832 | pubmed:author | pubmed-author:OhHidemasaH | lld:pubmed |
pubmed-article:18047832 | pubmed:author | pubmed-author:UeyamaTomomiT | lld:pubmed |
pubmed-article:18047832 | pubmed:author | pubmed-author:AsadaSatoshiS | lld:pubmed |
pubmed-article:18047832 | pubmed:author | pubmed-author:NakajimaNorio... | lld:pubmed |
pubmed-article:18047832 | pubmed:author | pubmed-author:NomuraTetsuya... | lld:pubmed |
pubmed-article:18047832 | pubmed:author | pubmed-author:TateishiKento... | lld:pubmed |
pubmed-article:18047832 | pubmed:author | pubmed-author:IsodonoKojiK | lld:pubmed |
pubmed-article:18047832 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18047832 | pubmed:day | 25 | lld:pubmed |
pubmed-article:18047832 | pubmed:volume | 365 | lld:pubmed |
pubmed-article:18047832 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18047832 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18047832 | pubmed:pagination | 863-9 | lld:pubmed |
pubmed-article:18047832 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
pubmed-article:18047832 | pubmed:meshHeading | pubmed-meshheading:18047832... | lld:pubmed |
pubmed-article:18047832 | pubmed:meshHeading | pubmed-meshheading:18047832... | lld:pubmed |
pubmed-article:18047832 | pubmed:meshHeading | pubmed-meshheading:18047832... | lld:pubmed |
pubmed-article:18047832 | pubmed:meshHeading | pubmed-meshheading:18047832... | lld:pubmed |
pubmed-article:18047832 | pubmed:meshHeading | pubmed-meshheading:18047832... | lld:pubmed |
pubmed-article:18047832 | pubmed:meshHeading | pubmed-meshheading:18047832... | lld:pubmed |
pubmed-article:18047832 | pubmed:meshHeading | pubmed-meshheading:18047832... | lld:pubmed |
pubmed-article:18047832 | pubmed:meshHeading | pubmed-meshheading:18047832... | lld:pubmed |
pubmed-article:18047832 | pubmed:meshHeading | pubmed-meshheading:18047832... | lld:pubmed |
pubmed-article:18047832 | pubmed:meshHeading | pubmed-meshheading:18047832... | lld:pubmed |
pubmed-article:18047832 | pubmed:meshHeading | pubmed-meshheading:18047832... | lld:pubmed |
pubmed-article:18047832 | pubmed:meshHeading | pubmed-meshheading:18047832... | lld:pubmed |
pubmed-article:18047832 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18047832 | pubmed:articleTitle | Skeletal muscle-derived progenitors capable of differentiating into cardiomyocytes proliferate through myostatin-independent TGF-beta family signaling. | lld:pubmed |
pubmed-article:18047832 | pubmed:affiliation | Department of Experimental Therapeutics, Translational Research Center, Kyoto University Hospital, Kyoto 606-8507, Japan. | lld:pubmed |
pubmed-article:18047832 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18047832 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:14313 | entrezgene:pubmed | pubmed-article:18047832 | lld:entrezgene |
entrez-gene:21803 | entrezgene:pubmed | pubmed-article:18047832 | lld:entrezgene |
http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:18047832 | lld:entrezgene |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:18047832 | lld:pubmed |