Cardiac-specific haploinsufficiency of beta-catenin attenuates cardiac hypertrophy but enhances fetal gene expression in response to aortic constriction.

Cardiac-specific haploinsufficiency of beta-catenin attenuates cardiac hypertrophy but enhances fetal gene expression in response to aortic constriction. Research Abstract Details 

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Cardiac-specific haploinsufficiency of beta-catenin attenuates cardiac hypertrophy but enhances fetal gene expression in response to aortic constriction. Abstract Text:

Jiaxiang Qu,Jibin Zhou,Xian Ping Yi,Baojun Dong,Hanqiao Zheng,Lisa M Miller,Xuejun Wang,Michael D Schneider,Faqian Li,

In addition to its role in cell adhesion, beta-catenin is an important signaling molecule in the Wnt/Wingless signaling pathway. Recent studies have indicated that beta-catenin is stabilized by hypertrophic stimuli and may regulate cardiac hypertrophic responses. To explore the role and requirement of beta-catenin in cardiac development and hypertrophy, we deleted the beta-catenin gene specifically in cardiac myocytes by crossing loxP-floxed beta-catenin mice with transgenic mice expressing a Cre recombinase under the control of the alpha-myosin heavy chain promoter. No homozygous beta-catenin-deleted mice were born alive and died before embryonic day 14.5, indicating significant and irreplaceable roles of beta-catenin in embryonic heart development. Heterozygous beta-catenin-deleted mice, however, demonstrated no structural and functional abnormality. The response of heterozygous beta-catenin-deleted mice to transverse aortic constriction, however, was significantly attenuated with decreased heart weight and heart weight/body weight ratio compared to controls with intact beta-catenin genes. Hemodynamic analysis revealed that there was no difference in cardiac function between wild-type and heterozygous beta-catenin-deleted mice. On the other hand, the expression of fetal genes, beta-myosin heavy chain, atrial and brain natriuretic peptides was significantly higher in heterozygous beta-catenin-deleted mice when compared to wild-type beta-catenin mice. These results suggest that the cytoplasmic level of beta-catenin modulates hypertrophic response and fetal gene reprogramming after pressure overload.

Cardiac-specific haploinsufficiency of beta-catenin attenuates cardiac hypertrophy but enhances fetal gene expression in response to aortic constriction. Publishing Authors By Initials

J Qu,J Zhou,XP Yi,B Dong,H Zheng,LM Miller,X Wang,MD Schneider,F Li,

For similar proteins: armadillo domain proteins: beta catenin research abstracts see: proteins: armadillo domain proteins: beta catenin research

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Cardiac-specific haploinsufficiency of beta-catenin attenuates cardiac hypertrophy but enhances fetal gene expression in response to aortic constriction. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of molecular and cellular cardiology

VOLUME: 43

Page Numbers: 319-26

Journal Abbreviation: J. Mol. Cell. Cardiol.

ISSN: 0022-2828

DAY: 21

MONTH: 06

YEAR: 2007

Cardiac-specific haploinsufficiency of beta-catenin attenuates cardiac hypertrophy but enhances fetal gene expression in response to aortic constriction. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 262322

Cardiac-specific haploinsufficiency of beta-catenin attenuates cardiac hypertrophy but enhances fetal gene expression in response to aortic constriction. Keywords Mesh Terms:

KEYWORDS: beta Catenin

MESH TERMS: metabolism

Chemical & Substance for Abstract: Cardiac-specific haploinsufficiency of beta-catenin attenuates cardiac hypertrophy but enhances fetal gene expression in response to aortic constriction. Information

Substance Name: beta Catenin

Registry Number: 0

Grant and Affiliation Information for Cardiac-specific haploinsufficiency of beta-catenin attenuates cardiac hypertrophy but enhances fetal gene expression in response to aortic constriction.

AFFILIATION: Sanford Research/USD, Cardiovascular Research Institute, Sanford School of Medicine of The University of South Dakota and Sanford Health, Sioux Falls, SD 57105, USA.

Country: England

AGENCY: United States NCRR

GRANT: P20 RR017662

ACRONYM: RR

MEDLINETA: J Mol Cell Cardiol

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