Genomic analysis distinguishes phases of early development of the mouse atrio-ventricular canal.

@article{Vrljicak2010GenomicAD,
  title={Genomic analysis distinguishes phases of early development of the mouse atrio-ventricular canal.},
  author={Pavle Vrljicak and Alex C Y Chang and Olena Morozova and Elizabeth D. Wederell and Kyle Niessen and Marco A. Marra and Aly Karsan and Pamela A. Hoodless},
  journal={Physiological genomics},
  year={2010},
  volume={40 3},
  pages={
          150-7
        }
}
Valve formation during embryonic heart development involves a complex interplay of regional specification, cell transformations, and remodeling events. While many studies have addressed the role of specific genes during this process, a global understanding of the genetic basis for the regional specification and development of the heart valves is incomplete. We have undertaken genome-wide transcriptional profiling of the developing heart valves in the mouse. Four Serial Analysis of Gene… 
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Results suggest that RBP-J-mediated Notch signaling in aortic valves may be critically involved in valve homeostasis and valve diseases as well, and will be helpful for the understanding of the molecular mechanisms of AVD in adults.
Genetic and functional genomics approaches targeting the Notch pathway in cardiac development and congenital heart disease.
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Functional data that implicates Notch in cardiac morphogenetic processes and expression profiling studies that enlighten the regulatory networks behind them are reviewed and a recurring theme is that Notch cross-talks reiteratively with other key signalling pathways to coordinate cell and tissue interactions during cardiogenesis.
Notch initiates the endothelial-to-mesenchymal transition in the atrioventricular canal through autocrine activation of soluble guanylyl cyclase.
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A human pluripotent stem cell-derived model fit to decode the early steps of human valvulogenesis and to recapitulate valve disease traits in a dish is developed and extended to patient specific iPS cells, revealing that dysregulation of the SHH pathway is likely to be at the origin of the disease thus providing a putative therapeutic target.
Transforming Growth Factor Beta3 is Required for Cardiovascular Development
TLDR
In vitro studies using TGFβ3-deficient fibroblasts in 3-D collagen lattice formation assays indicated that TGF β3 was required for collagen matrix reorganization, and biochemical studies indicated the ‘paradoxically’ increased activation of canonical (SMAD-dependent) and noncanonical (MAP kinase- dependent) pathways.
Human pre-valvular endocardial cells derived from pluripotent stem cells recapitulate cardiac pathophysiological valvulogenesis
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