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- W1989019781 abstract "Krüppel-like factor 4 (Klf4) is a transcription factor involved in differentiation and proliferation in multiple tissues. We demonstrated previously that tamoxifen-induced deletion of the <i>Klf4</i> gene in mice accelerated neointimal formation but delayed down-regulation of smooth muscle cell differentiation markers in carotid arteries following injury. To further determine the role of Klf4 in the cardiovascular system, we herein derived mice deficient for the <i>Klf4</i> gene in smooth and cardiac muscle using the <i>SM22</i>α promoter (<i>SM22</i>α-<i>CreKI</i><sup>+</sup>/<i>Klf4<sup>loxP/loxP</sup></i> mice). <i>SM22</i>α-<i>CreKI</i><sup>+</sup>/<i>Klf4<sup>loxP/loxP</sup></i> mice were born at the expected Mendelian ratio, but they gradually died after birth. Although ∼40% of <i>SM22</i>α-<i>CreKI</i><sup>+</sup>/<i>Klf4<sup>loxP/loxP</sup></i> mice survived beyond postnatal day 28, they exhibited marked growth retardation. In wild-type mice, Klf4 was expressed in the heart from late embryonic development through adulthood, whereas it was not expressed in smooth muscle. No changes were observed in morphology or expression of smooth muscle cell differentiation markers in vessels of <i>SM22</i>α-<i>CreKI</i><sup>+</sup>/<i>Klf4<sup>loxP/loxP</sup></i> mice. Of interest, cardiac output was significantly decreased in <i>SM22</i>α-<i>CreKI</i><sup>+</sup>/<i>Klf4<sup>loxP/loxP</sup></i> mice, as determined by magnetic resonance imaging. Moreover, a lack of Klf4 in the heart resulted in the reduction in expression of multiple cardiac genes, including <i>Gata4. In vivo</i> chromatin immunoprecipitation assays on the heart revealed that Klf4 bound to the promoter region of the <i>Gata4</i> gene. Results provide novel evidence that Klf4 plays a key role in late fetal and/or postnatal cardiac development." @default.
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- W1989019781 date "2010-07-01" @default.
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- W1989019781 title "Smooth and Cardiac Muscle-selective Knock-out of Krüppel-like Factor 4 Causes Postnatal Death and Growth Retardation" @default.
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- W1989019781 doi "https://doi.org/10.1074/jbc.m110.112482" @default.
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