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  • Title: Pressure and endothelial coculture upregulate myocytic Fas-FasL pathway and induce apoptosis by way of direct and paracrine mechanisms.
    Author: Vouyouka AG, Lin L, Basson MD.
    Journal: Am J Surg; 2005 Nov; 190(5):780-6. PubMed ID: 16226958.
    Abstract:
    BACKGROUND: Pressurized endothelial cell (EC)-smooth muscle cell (SMCs) coculture significantly increases the apoptosis of SMCs. Our current hypothesis was that in EC-SMC coculture, pressure upregulates SMC apoptosis SMCs through EC-derived paracrine factors and that SMC apoptosis is induced through Fas-Fas ligand (FasL) activation. METHODS: Conditioned media (CM) from ECs and SMCs exposed to ambient or high pressure was transferred to recipient SMCs. SMCs were stained with terminal deoxynucleotide transferase-mediated deoxy uridine triphosphate nick-end labeling. Fas and FasL expression was assessed in SMC grown in monoculture, coculture with EC, pressurized monoculture, and pressurized coculture with EC. RESULTS: CM from pressurized ECs caused a 30% increase in SMC apoptosis compared with CM from control ECs (P < .05). Pressure increased Fas and FasL expression in monocultured and cocultured SMCs (1.6-fold and 2.3-fold for Fas [P < .05] and 1.65-fold and 1.7-fold for FasL [P < or = .05]). Coculture had synergistic effect on Fas expression and no effect on FasL expression. CONCLUSIONS: Pressure plays significant role in EC-SMC interaction, SMC apoptosis, and vascular remodeling.
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