@article{RoedelAbdelilahSeyfried2021,
  author    = {R{\"o}del, Claudia Jasmin and Abdelilah-Seyfried, Salim},
  title     = {A zebrafish toolbox for biomechanical signaling in cardiovascular development and disease},
  series = {Current opinion in hematology},
  volume    = {28},
  journal   = {Current opinion in hematology},
  number    = {3},
  publisher = {Lippincott Williams \& Wilkins},
  address   = {Philadelphia},
  issn      = {1065-6251},
  doi       = {10.1097/MOH.0000000000000648},
  pages     = {198 -- 207},
  year      = {2021},
  abstract  = {Purpose of review The zebrafish embryo has emerged as a powerful model organism to investigate the mechanisms by which biophysical forces regulate vascular and cardiac cell biology during development and disease. A versatile arsenal of methods and tools is available to manipulate and analyze biomechanical signaling. This review aims to provide an overview of the experimental strategies and tools that have been utilized to study biomechanical signaling in cardiovascular developmental processes and different vascular disease models in the zebrafish embryo. Within the scope of this review, we focus on work published during the last two years. Recent findings Genetic and pharmacological tools for the manipulation of cardiac function allow alterations of hemodynamic flow patterns in the zebrafish embryo and various types of transgenic lines are available to report endothelial cell responses to biophysical forces. These tools have not only revealed the impact of biophysical forces on cardiovascular development but also helped to establish more accurate models for cardiovascular diseases including cerebral cavernous malformations, hereditary hemorrhagic telangiectasias, arteriovenous malformations, and lymphangiopathies. Summary The zebrafish embryo is a valuable vertebrate model in which in-vivo manipulations of biophysical forces due to cardiac contractility and blood flow can be performed. These analyses give important insights into biomechanical signaling pathways that control endothelial and endocardial cell behaviors. The technical advances using this vertebrate model will advance our understanding of the impact of biophysical forces in cardiovascular pathologies.},
  language  = {en}
}
@article{PaoliniFontanaVanCuongPhametal.2021,
  author    = {Paolini, Alessio and Fontana, Federica and Van-Cuong Pham, and R{\"o}del, Claudia Jasmin and Seyfried, Salim},
  title     = {Mechanosensitive Notch-Dll4 and Klf2-Wnt9 signaling pathways intersect in guiding valvulogenesis in zebrafish},
  series = {Cell reports},
  volume    = {37},
  journal   = {Cell reports},
  number    = {1},
  publisher = {Cell Press},
  address   = {Maryland Heights, MO},
  issn      = {2211-1247},
  doi       = {10.1016/j.celrep.2021.109782},
  pages     = {13},
  year      = {2021},
  abstract  = {In the zebrafish embryo, the onset of blood flow generates fluid shear stress on endocardial cells, which are specialized endothelial cells that line the interior of the heart. High levels of fluid shear stress activate both Notch and Klf2 signaling, which play crucial roles in atrioventricular valvulogenesis. However, it remains unclear why only individual endocardial cells ingress into the cardiac jelly and initiate valvulogenesis. Here, we show that lateral inhibition between endocardial cells, mediated by Notch, singles out Delta-like-4-positive endocardial cells. These cells ingress into the cardiac jelly, where they form an abluminal cell population. Delta-like-4-positive cells ingress in response to Wnt9a, which is produced in parallel through an Erk5Klf2-Wnt9a signaling cascade also activated by blood flow. Hence, mechanical stimulation activates parallel mechanosensitive signaling pathways that produce binary effects by driving endocardial cells toward either luminal or abluminal fates. Ultimately, these cell fate decisions sculpt cardiac valve leaflets.},
  language  = {en}
}