Currently, the laboratory is investigating the mechanisms behind the formation of vascular tumors and vascular anomalies through the identification of critical regulatory nodes that maintain vascular homeostasis and control endothelial proliferation...read more
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.
How Jagg1 (JAG1) expression is compartmentalized in the vascular plexus remains unclear. Our findings reveal an important feedforward loop whereby vascular endothelial growth factor (VEGF) stimulates zinc-finger protein 36 (ZFP36), consequently suppressing Jag1 to enable adequate levels of Notch signaling during sprouting angiogenesis.