Here we show that the emergence of aortic myeloid cells is not pathologically induced; instead, it is developmentally triggered as part of natural hemodynamic changes at birth that result in localized disturbed flow dynamics. Genetic ablation of this aortic myeloid resident population promotes fibrin deposition and microthrombus formation, clarifying its function as a critical regulator of hemostasis.
We performed single-cell RNA-sequencing of the ductus arteriosus in mouse embryos at E18.5, and neonatal stages P0.5, and P5 to identify transcriptional alterations that might be associated with remodeling.
We performed a high-content screen to identify drugs that block tumor cell extravasation by testing 3,520 compounds on a transendothelial invasion coculture assay. Our findings designate niclosamide as an effective drug that restricts tumor cell extravasation through modulation of signaling pathways, chemokines, and tumor-endothelial cell interactions.
Here we studied the molecular mechanisms of endothelial cell regeneration in adult vessels. Using a model of aortic injury, we found that regeneration occurs at the edges of the wounded area with equal strength and regardless of flow direction. Through a robust proliferative response, the wound closes by efforts of a rapidly dividing cell population that expresses Atf3.