Linked Life Data

20026769

Source:http://linkedlifedata.com/resource/pubmed/id/20026769

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2010-1-21
pubmed:abstractText
LIM domain proteins are important regulators in cell growth, cell fate determination, cell differentiation, and remodeling of the cell cytoskeleton. LIM and cysteine-rich domains 1 (Lmcd1) is a novel protein that contain 2 LIM domains with regular spacing in the carboxy-terminal region. However, its roles in cardiac growth remain unknown. Here, we investigated whether Lmcd1 regulates cardiac hypertrophy in vitro and in vivo and elucidated the underlying molecular mechanisms. We used primary cultured cardiac myocytes and cardiac-specific Lmcd1 transgenic mice. In wild-type mice subjected to the aortic banding, cardiac hypertrophy was evident at 8 weeks. In transgenic mice, however, cardiac hypertrophy was significantly greater than that in wild-type mice, as estimated by heart weight:body weight ratio, cardiomyocyte area, and echocardiographic measurements, as well as cardiac atrial natriuretic peptide and B-type natriuretic peptide mRNA and protein levels. Our results further showed that cardiac fibrosis observed in wild-type aortic banding mice was augmented in transgenic aortic banding mice. Importantly, calcineurin activity and nuclear factor of activated T cells activation level were increased more in transgenic mice than those in wild-type mice after 8-week aortic banding. In vitro experiments in cardiac myocytes further revealed that angiotensin II-induced calcineurin activity and nuclear factor of activated T cells activation were enhanced by overexpression but blunted by downregulation of Lmcd1. In conclusion, our results suggest that Lmcd1 plays a critical role in the development of cardiac hypertrophy via activation of calcineurin/nuclear factor of activated T cells signaling pathway.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
55
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
257-63
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:20026769-Animals, pubmed-meshheading:20026769-Blotting, Northern, pubmed-meshheading:20026769-Blotting, Western, pubmed-meshheading:20026769-Calcineurin, pubmed-meshheading:20026769-Cardiomegaly, pubmed-meshheading:20026769-Cells, Cultured, pubmed-meshheading:20026769-Cyclosporine, pubmed-meshheading:20026769-Disease Models, Animal, pubmed-meshheading:20026769-Drug Delivery Systems, pubmed-meshheading:20026769-Gene Expression Regulation, pubmed-meshheading:20026769-Homeodomain Proteins, pubmed-meshheading:20026769-LIM-Homeodomain Proteins, pubmed-meshheading:20026769-Mice, pubmed-meshheading:20026769-Mice, Transgenic, pubmed-meshheading:20026769-Myocytes, Cardiac, pubmed-meshheading:20026769-NFATC Transcription Factors, pubmed-meshheading:20026769-RNA, Messenger, pubmed-meshheading:20026769-Random Allocation, pubmed-meshheading:20026769-Signal Transduction, pubmed-meshheading:20026769-Transcription Factors, pubmed-meshheading:20026769-Transfection
pubmed:year
2010
pubmed:articleTitle
LIM and cysteine-rich domains 1 regulates cardiac hypertrophy by targeting calcineurin/nuclear factor of activated T cells signaling.
pubmed:affiliation
Department of Cardiology, Renmin Hospital, Wuhan University, Wuhan, People's Republic of China.
pubmed:publicationType
Journal Article, Comparative Study