| pubmed-article:20042608 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20042608 | lifeskim:mentions | umls-concept:C0026844 | lld:lifeskim |
| pubmed-article:20042608 | lifeskim:mentions | umls-concept:C1135918 | lld:lifeskim |
| pubmed-article:20042608 | lifeskim:mentions | umls-concept:C1522496 | lld:lifeskim |
| pubmed-article:20042608 | lifeskim:mentions | umls-concept:C0007595 | lld:lifeskim |
| pubmed-article:20042608 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:20042608 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:20042608 | lifeskim:mentions | umls-concept:C0031621 | lld:lifeskim |
| pubmed-article:20042608 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:20042608 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:20042608 | pubmed:issue | 13 | lld:pubmed |
| pubmed-article:20042608 | pubmed:dateCreated | 2010-3-22 | lld:pubmed |
| pubmed-article:20042608 | pubmed:abstractText | Proliferation of vascular smooth muscle cells (VSMCs) is a primary mechanism underlying cardiovascular proliferative disorders. Phosphoinositide 3-kinase (PI3K)-Akt (or protein kinase B) axis has been assigned at the center of pathways that regulate cell proliferation. Here we demonstrate that enhanced PI3K-Akt signaling by mitogenic stimulation or arterial injury profoundly elevates expression of receptor interacting protein 3 (RIP3) in primary cultured rat VSMCs and in vivo and that the up-regulation of RIP3 leads to VSMC growth arrest and apoptosis via inhibiting the PI3K-Akt signaling pathway, thereby alleviating balloon injury-induced neointimal formation. Specifically, mitogenic stimulation with platelet-derived growth factor-BB or angiotensin II leads to a profound increase in RIP3 expression, which is abolished by inhibition of PI3K or Akt, and increased PI3K-Akt signaling by expression of a constitutively active PI3K mutant also elevates RIP3 expression. Importantly, adenoviral overexpression of RIP3 not only triggers apoptosis but also causes cell cycle arrest at G(1)/G(0) phases that is associated with suppressed Akt activation. In sharp contrast, RIP3 gene silencing enhances serum- and platelet-derived growth factor-induced cell proliferation and Akt activation. In vivo adenoviral gene delivery of rat RIP3 (rRIP3) increased apoptosis and reduced VSMC proliferation, thus, effectively alleviating balloon injury-induced neointimal formation. The growth-suppressive and pro-apoptotic effects are independent of rRIP3 Ser/Thr kinase activity, because overexpression of a kinase-inactive mutant of rRIP3, similar to its wild type, is sufficient to induce growth arrest and apoptosis. These findings reveal a novel growth-suppressive action of RIP3, marking RIP3 as an important factor to prevent excessive mitogenic stimulation- or injury-induced vascular smooth muscle cells hyperplasia. | lld:pubmed |
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| pubmed-article:20042608 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20042608 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20042608 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20042608 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:20042608 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20042608 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:20042608 | pubmed:issn | 1083-351X | lld:pubmed |
| pubmed-article:20042608 | pubmed:author | pubmed-author:XiaoRui-PingR... | lld:pubmed |
| pubmed-article:20042608 | pubmed:author | pubmed-author:ZhengMingM | lld:pubmed |
| pubmed-article:20042608 | pubmed:author | pubmed-author:HEINHH | lld:pubmed |
| pubmed-article:20042608 | pubmed:author | pubmed-author:CaoChun-MeiCM | lld:pubmed |
| pubmed-article:20042608 | pubmed:author | pubmed-author:LiQianQ | lld:pubmed |
| pubmed-article:20042608 | pubmed:author | pubmed-author:ChenKuang-Hue... | lld:pubmed |
| pubmed-article:20042608 | pubmed:author | pubmed-author:LanXiaomeiX | lld:pubmed |
| pubmed-article:20042608 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20042608 | pubmed:day | 26 | lld:pubmed |
| pubmed-article:20042608 | pubmed:volume | 285 | lld:pubmed |
| pubmed-article:20042608 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20042608 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20042608 | pubmed:pagination | 9535-44 | lld:pubmed |
| pubmed-article:20042608 | pubmed:dateRevised | 2011-7-27 | lld:pubmed |
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