|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
14
|
|
pubmed:dateCreated |
2005-12-1
|
|
pubmed:abstractText |
The Src homology domain 2 (SH2)-containing tyrosine phosphatase-1 (SHP-1) plays a key role in apoptosis and decreases phosphorylation of Akt. Apoptosis of cardiomyocytes is thought to contribute to the increased area of acute myocardial infarction (AMI), and Akt activation exerts a powerful cardioprotective effect after ischemia. Thus, a therapeutic strategy designed to inhibit expression of SHP-1 would be beneficial in AMI. Here we report that siRNA targeting SHP-1 reduced infarct size in a rat model of AMI. Upon injection into the ischemic left ventricular wall, the vector-based siRNA significantly suppressed the increase in the SHP-1 mRNA and the SHP-1 protein levels. The siRNA vector also significantly reduced the SHP-1 that bound to Fas-R. The SHP-1 siRNA vector increased phospho-Akt and reduced DNA fragmentation and caspase activity compared with the scramble siRNA vector. Finally, the area of myocardial infarction was significantly smaller with the SHP-1 siRNA vector than with the scramble siRNA vector at 2 days after LCA ligation. In conclusion, SHP-1 in the heart increased from the early stage of AMI, and this increase was thought to contribute to the increased area of myocardial infarction. Suppression of SHP-1 with the SHP-1 siRNA vector markedly reduced the infarct size in AMI.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/Intracellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Phosphatase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Tyrosine Phosphatase...,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Tyrosine Phosphatases,
http://linkedlifedata.com/resource/pubmed/chemical/Ptpn6 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Dec
|
|
pubmed:issn |
1530-6860
|
|
pubmed:author |
|
|
pubmed:issnType |
Electronic
|
|
pubmed:volume |
19
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
2054-6
|
|
pubmed:dateRevised |
2007-11-15
|
|
pubmed:meshHeading |
pubmed-meshheading:16223786-Animals,
pubmed-meshheading:16223786-Antigens, CD95,
pubmed-meshheading:16223786-Apoptosis,
pubmed-meshheading:16223786-Blotting, Northern,
pubmed-meshheading:16223786-Blotting, Western,
pubmed-meshheading:16223786-Caspases,
pubmed-meshheading:16223786-Coronary Vessels,
pubmed-meshheading:16223786-DNA Fragmentation,
pubmed-meshheading:16223786-Echocardiography,
pubmed-meshheading:16223786-Gene Therapy,
pubmed-meshheading:16223786-Genetic Vectors,
pubmed-meshheading:16223786-Heart Ventricles,
pubmed-meshheading:16223786-Immunoprecipitation,
pubmed-meshheading:16223786-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:16223786-Male,
pubmed-meshheading:16223786-Models, Biological,
pubmed-meshheading:16223786-Myocardial Infarction,
pubmed-meshheading:16223786-Myocardial Ischemia,
pubmed-meshheading:16223786-Myocardium,
pubmed-meshheading:16223786-Myocytes, Cardiac,
pubmed-meshheading:16223786-Protein Phosphatase 1,
pubmed-meshheading:16223786-Protein Tyrosine Phosphatase, Non-Receptor Type 6,
pubmed-meshheading:16223786-Protein Tyrosine Phosphatases,
pubmed-meshheading:16223786-RNA, Messenger,
pubmed-meshheading:16223786-RNA, Small Interfering,
pubmed-meshheading:16223786-RNA Interference,
pubmed-meshheading:16223786-Rats,
pubmed-meshheading:16223786-Rats, Wistar,
pubmed-meshheading:16223786-Time Factors,
pubmed-meshheading:16223786-src Homology Domains
|
|
pubmed:year |
2005
|
|
pubmed:articleTitle |
RNA interference targeting SHP-1 attenuates myocardial infarction in rats.
|
|
pubmed:affiliation |
Department of Molecular and Cellular Biology, Division of Molecular and Clinical Gerontology, Medical Institute of Bioregulation, Kyushu University, Beppu, Oita, Japan.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
