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Calcyclin binding protein promotes DNA synthesis and differentiation in rat neonatal cardiomyocytes.

Authors: Au, KW  Kou, CY  Woo, AY  Chim, SS  Fung, KP  Cheng, CH  Waye, MM  Tsui, SK 
Citation: Au KW, etal., J Cell Biochem. 2006 Jun 1;98(3):555-66.
Pubmed: (View Article at PubMed) PMID:16440310
DOI: Full-text: DOI:10.1002/jcb.20710

During cardiac muscle development, most cardiomyocytes permanently withdraw from the cell cycle. Previously, by suppressive subtractive hybridization, we identified calcyclin-binding protein/Siah-interacting protein (CacyBP/SIP) as one of the candidates being upregulated in the hyperplastic to hypertrophic switch, suggesting an important role of CacyBP/SIP in cardiac development. To show the importance of CacyBP/SIP during myoblast differentiation, we report here that CacyBP/SIP is developmentally regulated in postnatal rat hearts. The overexpression of CacyBP/SIP promotes the differentiation and DNA synthesis of H9C2 cells and primary rat cardiomyocytes, as well as downregulates the expression of beta-catenin. Besides, CacyBP/SIP promotes the formation of myotubes and multinucleation upon differentiation. To investigate the cardioprotective role of CacyBP/SIP in cardiomyocytes, a hypoxia/reoxygenation model was employed. We found that CacyBP/SIP was upregulated during myocardial infarction (MI) and hypoxia/reoxygenation. As a conclusion, CacyBP/SIP may play a role in cardiomyogenic differentiation and possibly protection of cardiomyocytes during hypoxia/reoxygenation injury.


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CRRD Object Information
CRRD ID: 2326117
Created: 2010-06-24
Species: All species
Last Modified: 2010-06-24
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.