Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10754225 | Biochemical and Biophysical Research Communications | 2014 | 6 Pages |
Abstract
Recent studies have suggested glucagon-like peptide-1 (GLP-1) signaling to exert anti-inflammatory effects on endothelial cells, although the precise underlying mechanism remains to be elucidated. In the present study, we investigated whether PPARγ activation is involved in the GLP-1-mediated anti-inflammatory action on endothelial cells. When we treated HUVEC cells with 0.2 ng/ml exendin-4, a GLP-1 receptor agonist, endogenous PPARγ transcriptional activity was significantly elevated, by approximately 20%, as compared with control cells. The maximum PPARγ activity enhancing effect of exendin-4 was observed 12 h after the initiation of incubation with exendin-4. As H89, a PKA inhibitor, abolished GLP-1-induced PPARγ enhancement, the signaling downstream from GLP-1 cross-talk must have been involved in PPARγ activation. In conclusion, our results suggest that GLP-1 has the potential to induce PPARγ activity, partially explaining the anti-inflammatory effects of GLP-1 on endothelial cells. Cross-talk between GLP-1 signaling and PPARγ activation would have major impacts on treatments for patients at high risk for cardiovascular disease.
Keywords
pKaVCAM-1PAI-1IRS-1GLP-1HOMA-RNOX-1NF-κBPPARγHUVECICAM-1HUVECSGAPDHNADPHJnkTNFαc-Jun N-terminal kinasePPREinsulin receptor substrate-1tumor necrosis factor αHuman umbilical vein endothelial cellsperoxisome proliferator-activated receptor response elementNuclear factor-kappa Bplasminogen activator inhibitor 1intercellular adhesion molecule-1vascular cell adhesion molecule-1nicotinamide adenine dinucleotide phosphateprotein kinase Aglucagon-like peptide-1glyceraldehyde 3-phosphate dehydrogenase
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Authors
Hirohisa Onuma, Kouichi Inukai, Atsuko Kitahara, Rie Moriya, Susumu Nishida, Toshiaki Tanaka, Hidenori Katsuta, Kazuto Takahashi, Yoshikazu Sumitani, Toshio Hosaka, Hitoshi Ishida,