PDE4 inhibitor upregulates PTH-induced osteoclast formation via CRE-mediated COX-2 expression in osteoblasts

被引：12
|
作者：
Park, Hyojung [1 ]
No, A. Long Sae Mi [1 ]
Lee, Jung-Min [1 ]
Chen, Ling [1 ]
Lee, Soo Young [2 ]
Lee, Dong-Seok [3 ]
Yim, Mijung [1 ]
机构：
[1] Sookmyung Womens Univ, Coll Pharm, Seoul 140742, South Korea
[2] Ewha Womans Univ, Coll Nat Sci, Dept Life Sci, Seoul 120750, South Korea
[3] Kyungpook Natl Univ, Coll Nat Sci, Taegu 702701, South Korea
来源：
FEBS LETTERS | 2010年 / 584卷 / 01期
关键词：
Parathyroid hormone; Phosphodiesterase; 4; RANKL; COX-2; CRE; Osteoblast; Osteoclast; NECROSIS-FACTOR RECEPTOR; LIGAND; DIFFERENTIATION; KINASE; CELLS; PROTEIN; TRANCE/RANKL; INVOLVEMENT; BIOLOGY;
D O I：
10.1016/j.febslet.2009.11.043
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
We investigated the interplay between parathyroid hormone (PTH) and phosphodiesterases (PDEs) in osteoblasts. PDE4 negatively regulated PTH-induced cAMP accumulation. PDE4 inhibitor enhanced PTH-induced osteoclast formation and RANKL mRNA expression, which is partially mediated by COX-2 mRNA expression. Two CRE sites in the COX-2 promoter were required for the increase in COX-2 transcription by PDE4 inhibitor, and the expression of a dominant-negative form of CREB abolished COX-2 mRNA expression in response to PDE4 inhibitor or PTH in osteoblasts. Taken together, our data indicate that PDE4 inhibitor promotes PTH-induced osteoclast formation partially via CRE-mediated COX-2 mRNA expression. (C) 2009 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码：173 / 180
页数：8
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