Apoptosis of endothelial cells triggers a caspase-dependent anti-apoptotic paracrine loop active on VSMC MARC-ANDRÉ RAYMOND, ANIK DÉSORMEAUX, PATRICK LAPLANTE, NORMAND VIGNEAULT, JANOS G. FILEP † , KARINE LANDRY * , ALEXEY V. PSHEZHETSKY * and MARIE-JOSÉE HÉBERT 2 Research Centre CHUM, University of Montreal, East, Montreal, Canada; * Ste-Justine Hospital Research Centre, University of Montreal, Montreal, QC, Canada; and † Guy-Bernier Research Centre, Montreal, Canada 2 Correspondence: CRCHUM, 1560 Sherbrooke East, Montreal, QC, H2L 4M1, Canada. E-mail: marie-josee.hebert.chum@ssss.gouv.qc.ca <h3>SPECIFIC AIMS</h3> Increased endothelial apoptosis and decreased apoptosis of vascular smooth muscle cells (VSMC) are pivotal events for initiation of myo-intimal thickening. Yet mechanisms responsible for opposite regulations of apoptosis in endothelial and smooth muscle cells at sites of vascular injury are still largely undefined. We hypothesize that apoptosis of endothelial cells (EC) triggers the release of mediators, which in turn inhibit the apoptotic machinery of VSMC. <h3>PRINCIPAL FINDINGS</h3> <h3>1. Apoptosis of EC is associated with caspase-dependent release of paracrine anti-apoptotic factors for VSMC</h3> Apoptosis of human umbilical vein endothelial cells (HUVEC) was induced with serum starvation for 4 h. Then, serum-free medium conditioned by endothelial cells (SSC) was collected, centrifuged and used to serum starve rat transformed aortic VSMC
/lp/fed-of-american-socs-for-experimental-biology/apoptosis-of-endothelial-cells-triggers-a-caspase-dependent-anti-UBFB32Ocge