Pericyte actomyosin-mediated contraction at the cell–material interface can modulate the microvascular niche

摘要: Pericytes physically surround the capillary endothelium, contacting and communicating with associated vascular endothelial cells via cell?cell cell?matrix contacts. Pericyte?endothelial cell interactions thus have potential to modulate growth function of microvasculature. Here we employ experimental finding that pericytes can buckle a freestanding, underlying membrane actin-mediated contraction. were cultured on deformable silicone substrata, pericyte-generated wrinkles imaged both optical atomic force microscopy (AFM). The local stiffness subcellular domains near far from these was investigated by using AFM-enabled nanoindentation quantify effective elastic moduli. Substratum buckling contraction quantified normalized change in length initially flat regions substrata (corresponding wrinkle contour lengths), model used relate strain energies pericyte contractile forces. nature wrinkling protein-generated transduction further explored addition pharmacological cytoskeletal inhibitors affected forces moduli domains. Actin-mediated are sufficient for exert an average 38% elastomeric employed in?vitro studies. Actomyosin-mediated also act in?vivo compliant environment microvasculature, including basement other cells. Pericyte-generated substratum deformation serve as direct mechanical stimulus adjacent cells, potentially alter nonlinear extracellular matrices, pericyte?endothelial directly influence physiologic pathologic angiogenesis.