RGD Reference Report - Alpha B-crystallin suppresses pressure overload cardiac hypertrophy. - Rat Genome Database

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Alpha B-crystallin suppresses pressure overload cardiac hypertrophy.

Authors: Kumarapeli, AR  Su, H  Huang, W  Tang, M  Zheng, H  Horak, KM  Li, M  Wang, X 
Citation: Kumarapeli AR, etal., Circ Res. 2008 Dec 5;103(12):1473-82. Epub 2008 Oct 30.
RGD ID: 2303630
Pubmed: PMID:18974385   (View Abstract at PubMed)
PMCID: PMC2610480   (View Article at PubMed Central)
DOI: DOI:10.1161/CIRCRESAHA.108.180117   (Journal Full-text)

AlphaB-crystallin (CryAB) is the most abundant small heat shock protein (HSP) constitutively expressed in cardiomyocytes. Gain- and loss-of-function studies demonstrated that CryAB can protect against myocardial ischemia/reperfusion injury. However, the role of CryAB or any HSPs in cardiac responses to mechanical overload is unknown. This study addresses this issue. Nontransgenic mice and mice with cardiomyocyte-restricted transgenic overexpression of CryAB or with germ-line ablation of the CryAB/HSPB2 genes were subjected to transverse aortic constriction or sham surgery. Two weeks later, cardiac responses were analyzed by fetal gene expression profiling, cardiac function analyses, and morphometry. Comparison among the 3 sham surgery groups reveals that CryAB overexpression is benign, whereas the knockout is detrimental to the heart as reflected by cardiac hypertrophy and malfunction at 10 weeks of age. Compared to nontransgenic mice, transgenic mouse hearts showed significantly reduced NFAT transactivation and attenuated cardiac hypertrophic responses to transverse aortic constriction but unchanged cardiac function, whereas NFAT transactivation was significantly increased in cardiac and skeletal muscle of the knockout mice at baseline, and they developed cardiac insufficiency at 2 weeks after transverse aortic constriction. CryAB overexpression in cultured neonatal rat cardiomyocytes significantly attenuated adrenergic stimulation-induced NFAT transactivation and hypertrophic growth. We conclude that CryAB suppresses cardiac hypertrophic responses likely through attenuating NFAT signaling and that CryAB and/or HSPB2 are essential for normal cardiac function.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
negative regulation of cell growth  IDA 2303630 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Cryab  (crystallin, alpha B)


Additional Information