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Cardiac-Specific PID1 Overexpression Enhances Pressure Overload-Induced Cardiac Hypertrophy in Mice
- Source :
- Cellular Physiology and Biochemistry, Vol 35, Iss 5, Pp 1975-1985 (2015)
- Publication Year :
- 2015
- Publisher :
- Cell Physiol Biochem Press GmbH & Co KG, 2015.
-
Abstract
- Background/Aims: PID1 was originally described as an insulin sensitivity relevance protein, which is also highly expressed in heart tissue. However, its function in the heart is still to be elucidated. Thus this study aimed to investigate the role of PID1 in the heart in response to hypertrophic stimuli. Methods: Samples of human failing hearts from the left ventricles of dilated cardiomyopathy (DCM) patients undergoing heart transplants were collected. Transgenic mice with cardiomyocyte-specific overexpression of PID1 were generated, and cardiac hypertrophy was induced by transverse aortic constriction (TAC). The extent of cardiac hypertrophy was evaluated by echocardiography as well as pathological and molecular analyses of heart samples. Results: A significant increase in PID1 expression was observed in failing human hearts and TAC-treated wild-type mouse hearts. When compared with TAC-treated wild-type mouse hearts, PID1-TG mouse showed a significant exacerbation of cardiac hypertrophy, fibrosis, and dysfunction. Further analysis of the signaling pathway in vivo suggested that these adverse effects of PID1 were associated with the inhibition of AKT, and activation of MAPK pathway. Conclusion: Under pathological conditions, over-expression of PID1 promotes cardiac hypertrophy by regulating the Akt and MAPK pathway.
- Subjects :
- PID1
Cardiac hypertrophy
Akt
MAPK
Physiology
QP1-981
Biochemistry
QD415-436
Subjects
Details
- Language :
- English
- ISSN :
- 10158987, 14219778, and 00037400
- Volume :
- 35
- Issue :
- 5
- Database :
- Directory of Open Access Journals
- Journal :
- Cellular Physiology and Biochemistry
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.462173f2b584814856b9f6536f1ff26
- Document Type :
- article
- Full Text :
- https://doi.org/10.1159/000374005