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Calcyclin binding protein promotes DNA synthesis and differentiation in rat neonatal cardiomyocytes
Author(s) -
Au KaWing,
Kou Cecy Y.C.,
Woo Anthony Y.H.,
Chim Stephen S.C.,
Fung KwokPui,
Cheng Christopher H.K.,
Waye Mary M.Y.,
Tsui Stephen K.W.
Publication year - 2006
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20710
Subject(s) - myogenesis , downregulation and upregulation , myocyte , microbiology and biotechnology , suppression subtractive hybridization , cellular differentiation , hypoxia (environmental) , chemistry , biology , gene expression , biochemistry , gene , cdna library , organic chemistry , oxygen
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 β‐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. J. Cell. Biochem. 98: 555–566, 2006. © 2006 Wiley‐Liss, Inc.