TAILIEUCHUNG - Báo cáo khoa học: Novel suppression mechanism operating in early phase of adipogenesis by positive feedback loop for enhancement of cyclooxygenase-2 expression through prostaglandin F2a receptor mediated activation of MEK⁄ ERK-CREB cascade

Prostaglandin (PG) F2asuppresses adipocyte differentiation by inhibiting the function of peroxisome proliferator-activated receptor c. In this study, we identified a novel suppression mechanism, operating in the early phase of adipogenesis, that increased the production of anti-adipogenic PGF2a and PGE2by enhancing cyclooxygenase (COX) 2 | IFEBS Journal Novel suppression mechanism operating in early phase of adipogenesis by positive feedback loop for enhancement of cyclooxygenase-2 expression through prostaglandin F2a receptor mediated activation of MEK ERK-CREB cascade Toshiyuki Ueno and Ko Fujimori Laboratory of Biodefense and Regulation Osaka University of PharmaceuticalSciences Japan Keywords 3T3-L1 PGF2a adipocytes COX-2 CREB MEK ERK Correspondence K. Fujimori Laboratory of Biodefense and Regulation Osaka University of PharmaceuticalSciences 4-20-1 Nasahara Takatsuki Osaka 569-1094 Japan Fax 81 72 690 1215 Tel 81 72 690 1215 E-mail fujimori@ Received 6 April 2011 revised 31 May 2011 accepted 8 June 2011 doi Prostaglandin PG F2a suppresses adipocyte differentiation by inhibiting the function of peroxisome proliferator-activated receptor y. In this study we identified a novel suppression mechanism operating in the early phase of adipogenesis that increased the production of anti-adipogenic PGF2a and PGE2 by enhancing cyclooxygenase COX 2 expression through the PGF2a-activated FP receptor extracellular-signal-regulated kinase ERK cyclic AMP response element binding protein CREB cascade. COX-2 expression was enhanced with a peak at 1 h for the mRNA level and at 3 h for the protein level after the addition of Fluprostenol an FP receptor agonist. The Fluprostenol-derived elevation of COX-2 expression was suppressed by the co-treatment with an FP receptor antagonist AL8810 with a mitogen-activated protein kinase MEK ERK kinase inhibitor PD98059. ERK was phosphorylated within 10 min after the addition of Fluprostenol and its phosphorylation was inhibited by the co-treatment with AL8810 or PD98059. Moreover FP receptor mediated activation of the MEK ERK cascade and COX-2 expression increased the production of PGF2a and PGE2. An FP receptor antagonist and each inhibitor for MEK and COX-2 suppressed the PGF2a-derived induction of synthesis of these PGs. .

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