| First Author | Li L | Year | 2016 |
| Journal | Am J Transl Res | Volume | 8 |
| Issue | 4 | Pages | 1769-79 |
| PubMed ID | 27186301 | Mgi Jnum | J:240211 |
| Mgi Id | MGI:5882657 | Citation | Li L, et al. (2016) Cardiomyocyte specific deletion of PP2A causes cardiac hypertrophy. Am J Transl Res 8(4):1769-79 |
| abstractText | Cardiac hypertrophy is a common pathological alteration in heart disease, which has been reported to be connected with serine/threonine protein phosphatases that control the dephosphorylation of a variety of cardiac proteins. Herein, we generated protein phosphatase type 2A knockout expressing a tamoxifen-inducible Cre recombinase protein fused to two mutant estrogen-receptor ligand-binding domains (MerCreMer) under the control of the a-myosin heavy chain promoter. Cardiac function of mice was determined by echocardiography. Decrease in PP2A activity leads to increased cardiomyocyte hypertrophy and fibrosis. Loss of PP2ACalpha leads to the heart failure, including the changes of EF, FS, LV, ANP and BNP. On the molecular level, knockout mice shows increased expression of B55a and B56e at 60 days after tamoxifen injection. Additionally, the regulation of the Akt/GSK3beta/beta-catenin pathway is severely disturbed in knockout mice. In conclusion, cardiomyocyte specific deletion of PP2A gene causes the cardiac hypertrophy. We will use the knockout mice to generate a type of cardiomyocyte hypertrophy mouse model with myocardial fibrosis. |
