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(Circulation Research. 2006;98:715.)
© 2006 American Heart Association, Inc.

Editorials

GATA4 and the Two Sides of Gene Expression Reprogramming

Cinzia Perrino, Howard A. Rockman

From the Division of Cardiology (C.P.), Federico II University, Naples, Italy; and the Department of Medicine, Cell Biology and Molecular Genetics (H.A.R.), Duke University Medical Center, Durham, NC.

Correspondence to Howard A. Rockman, MD, Duke University Medical Center, DUMC Box 3104, Durham, NC 27710. E-mail h.rockman@duke.edu

See related article, pages 837–845

Key Words: GATA4 • gene expression • hypertrophy • heart failure • apoptosis

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
During embryonic development as well as in postnatal life, cardiac cells are continuously exposed to a host of extracellular signals to which they adapt and respond by activating intracellular signaling pathways and modulating the expression of nuclear genes. In the adult heart, the most common and easily recognized response to stressful stimuli is hypertrophy of cardiomyocytes and remodeling of the entire organ.¹ This reactive growth response requires de novo synthesis of contractile and structural proteins, obtained through a complex series of events culminating in gene expression reprogramming.²

GATA4 is a zinc-finger transcription factor highly expressed in cardiomyocytes at different developmental stages where it regulates the transcription of several structural and regulatory genes, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), - and ß-myosin heavy chain (MHC).³ In human hearts, GATA4 has also been demonstrated to be a critical regulator of cardiac development, as shown by the association between GATA4 mutations and the presence of congenital cardiac malformations.⁴ The specific effects of GATA4 deletion during embryonic age have been extensively investigated in genetically modified mouse models.^5–7 Mice homozygous for a GATA4 null allele⁶ or homozygous GATA4-deficient mice (GATA4^–/–)⁵ die early in development because of abnormal embryogenesis and heart tube formation. More recently, using a tetraploid embryo complementation strategy it has been possible to generate clonal embryonic day 9.5 Gata4^–/– embryos directly from embryonic stem cells and show that GATA4 is required for cardiogenesis.⁷ To date, however, because GATA4 is a critical regulator of cardiac morphogenesis, it has not been . . . [Full Text of this Article]

Related Article:

Cardiac-Specific Deletion of Gata4 Reveals Its Requirement for Hypertrophy, Compensation, and Myocyte Viability

Toru Oka, Marjorie Maillet, Alistair J. Watt, Robert J. Schwartz, Bruce J. Aronow, Stephen A. Duncan, and Jeffery D. Molkentin
Circ. Res. 2006 98: 837-845. [Abstract] [Full Text] [PDF]

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