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Compressive force inhibits adipogenesis through COX-2-mediated down-regulation of PPARγ2 and C/EBPα

Paper ID Volume ID Publish Year Pages File Format Full-Text
21470 43223 2010 7 PDF Available
Title
Compressive force inhibits adipogenesis through COX-2-mediated down-regulation of PPARγ2 and C/EBPα
Abstract

Various mechanical stimuli affect differentiation of mesoderm-derived cells such as osteoblasts or myoblasts, suggesting that adipogenesis may also be influenced by mechanical stimulation. However, effects of mechanical stimuli on adipogenesis are scarcely known. Compressive force was applied to a human preadipocyte cell line, SGBS. Levels of gene expression were estimated by real-time reverse transcription–polymerase chain reaction. The accumulation of lipids was evaluated by Sudan III or Oil Red O staining. In SGBS cells subjected to a compressive force of 226 Pa for 12 h before adipogenic induction, adipogenesis was inhibited. Compressive force immediately after adipogenic induction did not affect the adipogenesis. The expression of peroxisome proliferator-activated receptor (PPAR) γ2 and CCAAT/enhancer binding protein (C/EBP) α mRNA during adipogenesis was inhibited by compressive force, whereas C/EBPβ and C/EBPδ mRNA levels were unaffected. In preadipocytes, compressive force increased mRNA levels of Krüppel-like factor 2, preadipocyte factor 1, WNT10b, and cyclooxygenase-2 (COX-2) which are known as negative regulators for the PPARγ2 and C/EBPα genes. Furthermore, a COX-2 inhibitor completely reversed the inhibition of adipogenesis by compressive force. In conclusion, compressive force inhibited adipogenesis by suppressing expression of PPARγ2 and C/EBPα in a COX-2-dependent manner.

Keywords
Compressive force; Preadipocytes; Adipogenesis; COX-2; PPARγ2; C/EBPα
First Page Preview
Compressive force inhibits adipogenesis through COX-2-mediated down-regulation of PPARγ2 and C/EBPα
Publisher
Database: Elsevier - ScienceDirect
Journal: Journal of Bioscience and Bioengineering - Volume 109, Issue 3, March 2010, Pages 297–303
Authors
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Subjects
Physical Sciences and Engineering Chemical Engineering Bioengineering