NDLI: Peroxisome proliferator-activated receptor gamma down-regulates follistatin in intestinal epithelial cells through SP1.

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Peroxisome proliferator-activated receptor gamma down-regulates follistatin in intestinal epithelial cells through SP1.

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Peroxisome proliferator-activated receptor gamma down-regulates follistatin in intestinal epithelial cells through SP1.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Su, Weidong Thompson, E. Aubrey Necela, Brian M.
Description	Author Affiliation: Necela BM ( Department of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Jacksonville, Florida 32224, USA. necela.brian@mayo.edu)
Abstract	Activation of peroxisome proliferator-activated receptor gamma (PPARgamma) down-regulates the expression of follistatin mRNA in intestinal epithelial cells in vivo. The mechanism of PPARgamma-mediated down-regulation of follistatin was investigated using non-transformed, rat intestinal epithelial cells (RIE-1). RIE cells expressed activin A, the activin receptors ActRI and ActRII, and the follistatin-315 mRNA. RIE-1 cells responded to endogenous activin A, and this response was antagonized by follistatin, as evidenced by changes in cell growth and regulation of an activin-responsive reporter. Using RIE-1 cells, we show that activation of PPARgamma by rosiglitazone reduced follistatin mRNA levels in a dose- and concentration-dependent manner. Down-regulation of follistatin by rosiglitazone required the DNA binding domain of PPARgamma and was dependent upon dimerization with the retinoid X receptor. Inhibition of follistatin expression by rosiglitazone was not associated with decreased follistatin mRNA stability, suggesting that regulation may be at the promoter level. Analysis of the follistatin promoter revealed consensus binding sites for AP-1, AP-2, and Sp1. Targeting the AP-1 pathway with SP600125, an inhibitor of JNK, and TAM67, a dominant negative c-Jun, had no effect on PPARgamma-mediated down-regulation of follistatin. However, the follistatin promoter was dramatically regulated by Sp1, and this regulation was inhibited by PPARgamma expression. Knockdown of Sp1 expression relieved repression of follistatin levels by rosiglitazone. Moreover, PPARgamma was found to interact with Sp1 and repress its transcriptional activation function. Collectively, our data indicate that repression of Sp1 transcriptional activity by PPARgamma is the underlying mechanism responsible for PPARgamma-mediated regulation of follistatin expression.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	44
Volume Number	283
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2008-10-31
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Down-Regulation Epithelial Cells Metabolism Follistatin Biosynthesis Gene Expression Regulation Intestines PPAR Gamma Animals Anthracenes Pharmacology Enzyme Inhibitors MAP Kinase Kinase 4 Mice Mice, Inbred C57BL Models, Biological Thiazolidinediones Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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