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Plasticity of glucose‐dependent insulinotropic polypeptide (GIP) receptor expression in the vasculature
Author(s) -
Berglund Lisa M,
Kotova Olga,
Goncalves Isabel,
Kieffer Timothy J,
Lyssenko Valeriya,
Groop Leif,
Gomez Maria F
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1070.3
Subject(s) - medicine , endocrinology , incretin , gastric inhibitory polypeptide , biology , receptor , vascular smooth muscle , insulin , diabetes mellitus , glucagon , type 2 diabetes , smooth muscle
GIP and glucagon‐like peptide‐1 (GLP‐1) are the main incretin hormones secreted by the intestine after a meal. In addition to their insulinotropic activity, growing evidence suggests a cardioprotective role of GLP‐1, but much less is known about GIP‐signaling in this context. Here, we show using confocal immunohistochemistry that GIP receptor (GIPR) is expressed in intact arteries from human, mouse, rat and pig, predominantly in the endothelium but to a lesser extent also in the smooth muscle cell layer. Interestingly, GIPR mRNA determined by real‐time RT‐PCR increased in a time‐dependent manner in human microvascular endothelial cells (HMECs) upon serum starvation and in human coronary artery smooth muscle cells (HCASMCs) upon modulation towards a more proliferative phenotype, both characteristic events in vascular disease. High extracellular glucose enhanced GIPR mRNA expression in HCASMCs and this was prevented by the addition of insulin. Consistently, GIPR mRNA was higher in carotid arteries of diabetic Ins2Akita mice than in non‐diabetic controls. We also examined GIPR mRNA expression in 150 human carotid atherosclerotic plaques and found significantly elevated levels in patients with clinical symptoms. Collectively, these results suggest remarkable plasticity of GIPR expression of potential relevance for GIP‐signaling in the vasculature. Support: EASD, Swedish Heart & Lung Foundation.