Valve Interstitial Cells Act in a Pericyte Manner Promoting Angiogensis and Invasion by Valve Endothelial Cells.

Neovascularization is an understudied aspect of calcific aortic valve disease (CAVD). Within diseased valves, cells along the neovessels' periphery stain for pericyte markers, but it is unclear whether valvular interstitial cells (VICs) can demonstrate a pericyte-like phenotype. This investigation examined the perivascular potential of VICs to regulate valve endothelial cell (VEC) organization and explored the role of Angiopoeitin1-Tie2 signaling in this process.

Use of a functionalized introducer sheath and bioimpedance spectroscopy for real-time detection of vascular access complications.

Internal bleeding complications (IBCs) occurring at vascular access sites are associated with worsening patient outcomes and increased costs. This study assessed the IBC detection capabilities of a bioimpedance spectroscopy (BS) monitoring system that uses a novel functionalized introducer sheath. The device was tested in three large animal models of a clinical IBC.

Regulation of valve endothelial cell vasculogenic network architectures with ROCK and Rac inhibitors.

Objective: The age- and disease-dependent presence of microvessels within heart valves is an understudied characteristic of these tissues. Neovascularization involves endothelial cell (EC) migration and cytoskeletal reorientation, which are heavily regulated by the Rho family of GTPases. Given that valve ECs demonstrate unique mesenchymal transdifferentiation and cytoskeletal mechanoresponsiveness, compared to vascular ECs, this study quantified the effect of inhibiting two members of the Rho family on vasculogenic network formation by valve ECs.