Abstract | BACKGROUND: METHOD: We established transgenic mice (TG) ubiquitously over-expressing human CAST protein and produced MI in TG mice and C57BL/6J wild-type (WT) littermates. RESULTS: The CAST protein expression was profoundly upregulated in the myocardial tissue of TG mice compared with WT littermates (P < 0.01). Overexpression of CAST significantly reduced the infarct size (P < 0.01) and blunted MI-induced interventricular hypertrophy, global myocardial fibrosis and collagen I and collagen III deposition, hypotension and hemodynamic disturbances at 21 days after MI. Moreover, the MI-induced up-regulation and activation of calpains were obviously attenuated in CAST TG mice. MI-induced down-regulation of CAST was partially reversed in TG mice. Additionally, the MI-caused imbalance of matrix metalloproteinases and their inhibitors was improved in TG mice. CONCLUSIONS:
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Authors | Tingqiao Ye, Qiang Wang, Yan Zhang, Xiaofeng Song, Dachun Yang, De Li, Dan Li, Linan Su, Yongjian Yang, Shuangtao Ma |
Journal | PloS one
(PLoS One)
Vol. 10
Issue 3
Pg. e0120178
( 2015)
ISSN: 1932-6203 [Electronic] United States |
PMID | 25786109
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Collagen Type I
- Collagen Type III
- Cytoskeletal Proteins
- Erc2 protein, mouse
- Isoenzymes
- Matrix Metalloproteinase Inhibitors
- Calpain
- Matrix Metalloproteinases, Secreted
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Topics |
- Animals
- Calpain
(genetics, metabolism)
- Cardiomegaly
(enzymology, genetics, mortality, pathology)
- Collagen Type I
(genetics, metabolism)
- Collagen Type III
(genetics, metabolism)
- Cytoskeletal Proteins
(genetics, metabolism)
- Disease Models, Animal
- Enzyme Activation
- Female
- Fibrosis
- Gene Expression Regulation
- Humans
- Isoenzymes
(genetics, metabolism)
- Male
- Matrix Metalloproteinase Inhibitors
(metabolism)
- Matrix Metalloproteinases, Secreted
(genetics, metabolism)
- Mice
- Mice, Inbred C57BL
- Mice, Transgenic
- Myocardial Infarction
(enzymology, genetics, mortality, pathology)
- Survival Analysis
- Ventricular Function, Left
(genetics)
- Ventricular Remodeling
(genetics)
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