@article{RenzOttenFaurobertetal.2015,
  author    = {Renz, Marc and Otten, Cecile and Faurobert, Eva and Rudolph, Franziska and Zhu, Yuan and Boulday, Gwenola and Duchene, Johan and Mickoleit, Michaela and Dietrich, Ann-Christin and Ramspacher, Caroline and Steed, Emily and Manet-Dupe, Sandra and Benz, Alexander and Hassel, David and Vermot, Julien and Huisken, Jan and Tournier-Lasserve, Elisabeth and Felbor, Ute and Sure, Ulrich and Albiges-Rizo, Corinne and Abdelilah-Seyfried, Salim},
  title     = {Regulation of beta 1 Integrin-Klf2-Mediated angiogenesis by CCM proteins},
  series = {Developmental cell},
  volume    = {32},
  journal   = {Developmental cell},
  number    = {2},
  publisher = {Cell Press},
  address   = {Cambridge},
  issn      = {1534-5807},
  doi       = {10.1016/j.devcel.2014.12.016},
  pages     = {181 -- 190},
  year      = {2015},
  abstract  = {Mechanotransduction pathways are activated in response to biophysical stimuli during the development or homeostasis of organs and tissues. In zebrafish, the blood-flow-sensitive transcription factor Klf2a promotes VEGF-dependent angiogenesis. However, the means by which the Klf2a mechanotransduction pathway is regulated to prevent continuous angiogenesis remain unknown. Here we report that the upregulation of klf2 mRNA causes enhanced egfl7 expression and angiogenesis signaling, which underlies cardiovascular defects associated with the loss of cerebral cavernous malformation (CCM) proteins in the zebrafish embryo. Using CCM-protein-depleted human umbilical vein endothelial cells, we show that the misexpression of KLF2 mRNA requires the extracellular matrix-binding receptor beta 1 integrin and occurs in the absence of blood flow. Downregulation of beta 1 integrin rescues ccm mutant cardiovascular malformations in zebrafish. Our work reveals a beta 1 integrin-Klf2-Egfl7-signaling pathway that is tightly regulated by CCM proteins. This regulation prevents angiogenic overgrowth and ensures the quiescence of endothelial cells.},
  language  = {en}
}
@article{DietrichLombardoAbdelilahSeyfried2014,
  author    = {Dietrich, Ann-Christin and Lombardo, Veronica A. and Abdelilah-Seyfried, Salim},
  title     = {Blood flow and Bmp signaling control endocardial chamber morphogenesis},
  series = {Developmental cell},
  volume    = {30},
  journal   = {Developmental cell},
  number    = {4},
  publisher = {Cell Press},
  address   = {Cambridge},
  issn      = {1534-5807},
  doi       = {10.1016/j.devcel.2014.06.020},
  pages     = {367 -- 377},
  year      = {2014},
  abstract  = {During heart development, the onset of heartbeat and blood flow coincides with a ballooning of the cardiac chambers. Here, we have used the zebrafish as a vertebrate model to characterize chamber ballooning morphogenesis of the endocardium, a specialized population of endothelial cells that line the interior of the heart. By combining functional manipulations, fate mapping studies, and high-resolution imaging, we show that endocardial growth occurs without an influx of external cells. Instead, endocardial cell proliferation is regulated, both by blood flow and by Bmp signaling, in a manner independent of vascular endothelial growth factor (VEGF) signaling. Similar to myocardial cells, endocardial cells obtain distinct chamber-specific and inner- versus outer-curvature-specific surface area sizes. We find that the hemodynamic-sensitive transcription factor Klf2a is involved in regulating endocardial cell morphology. These findings establish the endocardium as the flow-sensitive tissue in the heart with a key role in adapting chamber growth in response to the mechanical stimulus of blood flow.},
  language  = {en}
}