Prdm6 Is Essential for Cardiovascular Development In Vivo

Andreas Gewies(Technical University of Munich), Mercedes Castiñeiras-Vilariño(Technical University of Munich), Uta Ferch(Klinikum rechts der Isar), Nina Jährling(TU Wien), Katja Heinrich(Klinikum rechts der Isar), Ulrike Hoeckendorf(Technical University of Munich), Gerhard K. H. Przemeck(Helmholtz Zentrum München), Matthias Munding(Helmholtz Zentrum München), Olaf Groß(Klinikum rechts der Isar), Timm Schroeder(Helmholtz Zentrum München), Marion Horsch(Helmholtz Zentrum München), E. Loraine Karran(MRC Toxicology Unit), Aneela Majid(University of Leicester), Stefan Antonowicz(University of Leicester), Johannes Beckers(Technical University of Munich), Martin Hrabě de Angelis(Helmholtz Zentrum München), Hans‐Ulrich Dodt(TU Wien), Christian Peschel(Technical University of Munich), Irmgard Förster(Technical University of Munich), Martin J.S. Dyer(University of Leicester), Jürgen Ruland(Heidelberg University)
PLoS ONE
November 21, 2013
Cited by 21Open Access
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Abstract

Members of the PRDM protein family have been shown to play important roles during embryonic development. Previous in vitro and in situ analyses indicated a function of Prdm6 in cells of the vascular system. To reveal physiological functions of Prdm6, we generated conditional Prdm6-deficient mice. Complete deletion of Prdm6 results in embryonic lethality due to cardiovascular defects associated with aberrations in vascular patterning. However, smooth muscle cells could be regularly differentiated from Prdm6-deficient embryonic stem cells and vascular smooth muscle cells were present and proliferated normally in Prdm6-deficient embryos. Conditional deletion of Prdm6 in the smooth muscle cell lineage using a SM22-Cre driver line resulted in perinatal lethality due to hemorrhage in the lungs. We thus identified Prdm6 as a factor that is essential for the physiological control of cardiovascular development.


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