This suggests thatĮgfl7is vital for the formation of endothelial cell cords, and that the gene has an important role during both vasculogenesis and angiogenesis in mammalian cells.Įgfl7, was identified in a screen for genes with restricted expression during In conclusion, our work shows that knock-down ofĮgfl7causes defects in early vascular cord formation, and results in the development of CD31+ sheet-like structures. Cell death within EBs was unaffected byĮgfl7knock-down. Formation of these sheets was due, at least in part, to increased proliferation specifically of CD31+ cells. A partial remodelling occurred by 14 days of differentiation when fewer CD31+ sheets were seen both within EBs, and as outgrowths from EBs. Similar CD31+ sheets were also seen as outgrowths from 7 day EBs into collagen gels. Only up to 60% of these sheets co-expressed basement membrane and endothelial cell junction markers. Knock-down ofĮgfl7resulted in the formation of abnormal sheet-like CD31+ structures that were abundant within EBs after 7 days of differentiation. In vitroembryoid body (EB) model after either 7 or 14 days of differentiation. Here we use an siRNA knock-down approach to target specific regions ofĮgfl7was knocked down in mouse ESCs and the effect on vascular development was assessed using the MiR-126, an intronic microRNA located withinĮgfl7, results in vascular defects. ![]() Interpretation of mouse knockout studies has been complicated by the fact that deletion of While it has been shown thatĮgfl7knock-down in zebrafish impairs endothelial cord formation, the role of the gene in mammals has been unresolved. ![]() Egfl7, is a largely endothelial restricted gene which is thought to have a role during the differentiation of embryonic stem cells (ESCs) along the endothelial lineage.
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