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ShareScienceDaily (Dec. 13, 2007) — Injury to the human heart, such as caused by high blood pressure and heart attack, results in the enlargement of heart muscle cells (cardiomyocyte hypertrophy) and the activation of a fetal program of cardiac gene expression.
This pathological response leads to heart failure and death. On a molecular level, this pathological response is driven by enhanced expression of genes in response to the presence of proteins named transcription factors, including the MEF2 family of transcription factors.
However, whether the MEF2 transcription factors are required for heart disease to occur had not been determined. A new study by Eric Olsen and his colleagues at the University of Texas Southwestern Medical Center, Dallas, has now revealed a unique role for MEF2D in regulating the pathological cardiac response to stress in adult mouse hearts.
The researchers generated mice deficient in MEF2D, and found that hearts from these mice exhibited blunted responses to cardiac stress.
In particular, pressure overload in the hearts of these mice resulted in reduced cardiomyocyte hypertrophy, fetal gene activation, and scarring compared with normal mice. Similar results were seen when cardiac stress was induced with injection of a drug known to cause these conditions.
In contrast, overproduction of MEF2D in mice resulted in profound heart disease, evidenced by extensive scarring of the heart tissue, heart dilation, pathological blood clotting, and severely congested lungs and liver. Because MEF2 transcription factors are found in almost all the tissues in the body, the authors concluded from these data that in addition to affecting stress-induced remodeling of the heart, altering MEF2 protein expression might also be a useful therapy for various noncardiac diseases.
Journal article: The MEF2D transcription factor mediates stress-dependent cardiac remodeling in mice. Journal of Clinical Investigation. Dec 13, 2007.
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The above story is reprinted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.
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