کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10754225 | 1050351 | 2014 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The glucagon-like peptide 1 receptor agonist enhances intrinsic peroxisome proliferator-activated receptor γ activity in endothelial cells
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کلمات کلیدی
pKaVCAM-1PAI-1IRS-1GLP-1HOMA-RNOX-1NF-κBPPARγHUVECICAM-1HUVECSGAPDHNADPHJnkTNFαc-Jun N-terminal kinase - C-Jun N-terminal kinasePPRE - ارسالinsulin receptor substrate-1 - انسولین گیرنده زیربخش 1tumor necrosis factor α - تومور نکروز عامل αHuman umbilical vein endothelial cells - سلول های اندوتلیالی ورید ناف انسانperoxisome proliferator-activated receptor response element - عنصر پاسخ گیرنده فعال پرولیفراسیون فعالNuclear factor-kappa B - فاکتور هسته ای-کاپا Bplasminogen activator inhibitor 1 - مهار کننده فعال کننده پلاسمینوژن 1intercellular adhesion molecule-1 - مولکول چسبندگی بین سلولی -1vascular cell adhesion molecule-1 - مولکول چسبندگی سلولی عروقی-1nicotinamide adenine dinucleotide phosphate - نیکوتین آمید adenine dinucleotide phosphateprotein kinase A - پروتئین کیناز Aglucagon-like peptide-1 - پپتید 1-گلوکاگون-مانندglyceraldehyde 3-phosphate dehydrogenase - گلیسرولیدید 3-فسفات دهیدروژناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 451, Issue 2, 22 August 2014, Pages 339-344
Journal: Biochemical and Biophysical Research Communications - Volume 451, Issue 2, 22 August 2014, Pages 339-344
نویسندگان
Hirohisa Onuma, Kouichi Inukai, Atsuko Kitahara, Rie Moriya, Susumu Nishida, Toshiaki Tanaka, Hidenori Katsuta, Kazuto Takahashi, Yoshikazu Sumitani, Toshio Hosaka, Hitoshi Ishida,