کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2196043 | 1550894 | 2014 | 11 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Termination mechanism of CREB-dependent activation of COX-2 expression in early phase of adipogenesis Termination mechanism of CREB-dependent activation of COX-2 expression in early phase of adipogenesis](/preview/png/2196043.png)
• IBMX elevated the activity of PKA.
• dbcAMP enhanced the phosphorylation of CREB through activation of PKA.
• CREB siRNA suppressed the expression of the COX-2.
• Okadaic acid repressed the adipogenesis by elevating CREB-dependent COX-2 expression.
We elucidated the molecular mechanism of prostaglandin (PG) E2- and PGF2α-mediated suppression of the early phase of adipogenesis through enhanced COX-2 expression in 3T3-L1 cells. 3-Isobutyl-1-methylxanthine, an inhibitor of phosphodiesterase which catalyzes the conversion of cAMP to AMP, enhanced the activity of protein kinase A (PKA). Dibutyryl cAMP activated PKA and enhanced the phosphorylation of cAMP response element (CRE)-binding protein (CREB). The ability of CREB binding to the CRE of the COX-2 promoter was elevated for enhancement of the expression of the COX-2 gene. CREB siRNA suppressed the expression of the COX-2 gene. Furthermore, okadaic acid, a protein phosphatase (PP) 1/2A inhibitor, suppressed the progression of adipogenesis by preventing PP1/2A-mediated suppression of CREB-dependent COX-2 expression, thus resulting in increased production of anti-adipogenic PGE2 and PGF2α. These results indicate that CREB-dependent expression of COX-2 for the production of anti-adipogenic PGs is critical for the regulation of the early phase of adipogenesis.
Journal: Molecular and Cellular Endocrinology - Volume 384, Issues 1–2, 25 March 2014, Pages 12–22