Pressure and endothelial coculture upregulate myocytic Fas–FasL pathway and induce apoptosis by way of direct and paracrine mechanisms - 18/08/11
, Lifeng Lin, M.S. a, b, Marc D. Basson, M.D., Ph.D. a, b
Corresponding author. Tel.: +1-313-576-3982; fax: +1-313-576-1002.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 ≤.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.
Le texte complet de cet article est disponible en PDF.Keywords : Apoptosis, Fas–Fas ligand, Flow cytometry, Smooth muscle cell–endothelial cell coculture
Plan
Vol 190 - N° 5
P. 780-786 - novembre 2005 Retour au numéro
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