CIP4 is required for the hypertrophic growth of neonatal cardiac myocytes

Journal of Biomedical Science

Michael S Kapiloff¹  Jinliang Li¹  Hrishikesh Thakur¹  Francesca Rusconi¹ 

[1] Cardiac Signal Transduction and Cellular Biology Laboratory, Interdisciplinary Stem Cell Institute, Departments of Pediatrics and Medicine, Leonard M. Miller School of Medicine, University of Miami, R198, P.O. Box 016960, Miami, FL 33101, USA

关键词: Myocyte;    Hypertrophy;    Heart;    CIP4;   

Others  :  823469
DOI  :  10.1186/1423-0127-20-56

 received in 2013-05-28, accepted in 2013-08-01,  发布年份 2013

【 摘 要 】

Background

CIP4 is a scaffold protein that regulates membrane deformation and tubulation, organization of the actin cytoskeleton, endocytosis of growth factor receptors, and vesicle trafficking. Although expressed in the heart, CIP4 has not been studied with regards to its potential function in cardiac myocytes.

Results

We now show using RNA interference that CIP4 expression in neonatal rat ventricular myocytes is required for the induction of non-mitotic, hypertrophic growth by the α-adrenergic agonist phenylephrine, the IL-6 cytokine leukemia inhibitor factor, and fetal bovine serum, as assayed using morphometry, immunocytochemistry for the hypertrophic marker atrial natriuretic factor and [³H]leucine incorporation for de novo protein synthesis. This requirement was consistent with the induction of CIP4 expression by hypertrophic stimulation. The inhibition of myocyte hypertrophy by CIP4 small interfering oligonucleotides (siRNA) was rescued by expression of a recombinant CIP4 protein, but not by a mutant lacking the N-terminal FCH domain responsible for CIP4 intracellular localization.

Conclusions

These results imply that CIP4 plays a significant role in the intracellular hypertrophic signal transduction network that controls the growth of cardiac myocytes in heart disease.

【 授权许可】

   
2013 Rusconi et al.; licensee BioMed Central Ltd.

【 图 表 】

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