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新虫 (小有名气)

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虫号: 1686633
注册: 2012-03-13
专业: 基因组学

[求助] 求大神帮忙翻译文献摘要

Cardiac malformations due to aberrant development of the atrioventricular (AV) valves are among the most common forms of
congenital heart disease. At localized swellings of extracellular matrix known as the endocardial cushions, the endothelial lining of
the heart undergoes an epithelial to mesenchymal transition (EMT) to form the mesenchymal progenitors of the AV valves. Further
growth and differentiation of these mesenchymal precursors results in the formation of portions of the atrial and ventricular
septae, and the generation of thin, pliable valves. Gata4, which encodes a zinc finger transcription factor, is expressed in the
endothelium and mesenchyme of the AV valves. Using a Tie2-Cre transgene, we selectively inactivated Gata4 within endothelialderived
cells. Mutant endothelium failed to undergo EMT, resulting in hypocellular cushions. Mutant cushions had decreased levels
of Erbb3, an EGF-family receptor essential for EMT in the atrioventricular cushions. In Gata4 mutant embryos, Erbb3
downregulation was associated with impaired activation of Erk, which is also required for EMT. Expression of a Gata4 mutant
protein defective in interaction with Friend of Gata (FOG) cofactors rescued the EMT defect, but resulted in a decreased
proliferation of mesenchyme and hypoplastic cushions that failed to septate the ventricular inlet. We demonstrate two novel
functions of Gata4 in development of the AV valves. First, Gata4 functions as an upstream regulator of an Erbb3-Erk pathway
necessary for EMT, and second, Gata4 acts to promote cushion mesenchyme growth and remodeling.
求这段的翻译复试用拜托啦

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