| pubmed-article:20023119 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20023119 | lifeskim:mentions | umls-concept:C0026844 | lld:lifeskim |
| pubmed-article:20023119 | lifeskim:mentions | umls-concept:C0003018 | lld:lifeskim |
| pubmed-article:20023119 | lifeskim:mentions | umls-concept:C0006776 | lld:lifeskim |
| pubmed-article:20023119 | lifeskim:mentions | umls-concept:C2265909 | lld:lifeskim |
| pubmed-article:20023119 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:20023119 | lifeskim:mentions | umls-concept:C1556066 | lld:lifeskim |
| pubmed-article:20023119 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
| pubmed-article:20023119 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
| pubmed-article:20023119 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:20023119 | pubmed:dateCreated | 2010-1-21 | lld:pubmed |
| pubmed-article:20023119 | pubmed:abstractText | Despite our understanding that medial smooth muscle hypertrophy is a central feature of vascular remodeling, the molecular pathways underlying this pathology are still not well understood. Work over the past decade has illustrated a potential role for the multifunctional calmodulin-dependent kinase CaMKII in smooth muscle cell contraction, growth, and migration. Here we demonstrate that CaMKII is enriched in vascular smooth muscle (VSM) and that CaMKII inhibition blocks ANG II-dependent VSM cell hypertrophy in vitro and in vivo. Specifically, systemic CaMKII inhibition with KN-93 prevented ANG II-mediated hypertension and medial hypertrophy in vivo. Adenoviral transduction with the CaMKII peptide inhibitor CaMKIIN abrogated ANG II-induced VSM hypertrophy in vitro, which was augmented by overexpression of CaMKII-delta2. Finally, we identify the downstream signaling components critical for ANG II- and CaMKII-mediated VSM hypertrophy. Specifically, we demonstrate that CaMKII induces VSM hypertrophy by regulating histone deacetylase 4 (HDAC4) activity, thereby stimulating activity of the hypertrophic transcription factor MEF2. MEF2 transcription is activated by ANG II in vivo and abrogated by the CaMKII inhibitor KN-93. Together, our studies identify a complete pathway for ANG II-triggered arterial VSM hypertrophy and identify new potential therapeutic targets for chronic human hypertension. | lld:pubmed |
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| pubmed-article:20023119 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20023119 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20023119 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20023119 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20023119 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:20023119 | pubmed:issn | 1522-1539 | lld:pubmed |
| pubmed-article:20023119 | pubmed:author | pubmed-author:FoàVV | lld:pubmed |
| pubmed-article:20023119 | pubmed:author | pubmed-author:MohlerPeter... | lld:pubmed |
| pubmed-article:20023119 | pubmed:author | pubmed-author:AndersonMark... | lld:pubmed |
| pubmed-article:20023119 | pubmed:author | pubmed-author:GuptaArun KAK | lld:pubmed |
| pubmed-article:20023119 | pubmed:author | pubmed-author:LiWeiweiW | lld:pubmed |
| pubmed-article:20023119 | pubmed:author | pubmed-author:GrumbachIsabe... | lld:pubmed |
| pubmed-article:20023119 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20023119 | pubmed:volume | 298 | lld:pubmed |
| pubmed-article:20023119 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20023119 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20023119 | pubmed:pagination | H688-98 | lld:pubmed |
| pubmed-article:20023119 | pubmed:dateRevised | 2011-10-14 | lld:pubmed |
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