@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{LombardoOttenAbdelilahSeyfried2015,
  author    = {Lombardo, Veronica A. and Otten, Cecile and Abdelilah-Seyfried, Salim},
  title     = {Large-scale Zebrafish Embryonic Heart Dissection for Transcriptional Analysis},
  series = {Journal of visualized experiments},
  journal   = {Journal of visualized experiments},
  number    = {95},
  publisher = {JoVE},
  address   = {Cambridge},
  issn      = {1940-087X},
  doi       = {10.3791/52087},
  pages     = {7},
  year      = {2015},
  abstract  = {The zebrafish embryonic heart is composed of only a few hundred cells, representing only a small fraction of the entire embryo. Therefore, to prevent the cardiac transcriptome from being masked by the global embryonic transcriptome, it is necessary to collect sufficient numbers of hearts for further analyses. Furthermore, as zebrafish cardiac development proceeds rapidly, heart collection and RNA extraction methods need to be quick in order to ensure homogeneity of the samples. Here, we present a rapid manual dissection protocol for collecting functional/beating hearts from zebrafish embryos. This is an essential prerequisite for subsequent cardiac-specific RNA extraction to determine cardiac-specific gene expression levels by transcriptome analyses, such as quantitative real-time polymerase chain reaction (RT-qPCR). The method is based on differential adhesive properties of the zebrafish embryonic heart compared with other tissues; this allows for the rapid physical separation of cardiac from extracardiac tissue by a combination of fluidic shear force disruption, stepwise filtration and manual collection of transgenic fluorescently labeled hearts.},
  language  = {en}
}