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diabetes beta arrestin2

Hyunjin Noh, Mi Ra Yu, Hyun Joo Kim, Ji Hye Lee, Byoung-Won Park, I-Hsien Wu, Motonobu Matsumoto, George L King
Macrophage activation is increased in diabetes and correlated with the onset and progression of vascular complications. To identify drugs that could inhibit macrophage activation, we developed a cell-based assay and screened a 1,040 compound library for anti-inflammatory effects. Beta2-adrenergic receptor (β2AR) agonists were identified as the most potent inhibitors of phorbol myristate acetate-induced tumor necrosis factor-α production in rat bone marrow macrophages. In peripheral blood mononuclear cells isolated from streptozotocin-induced diabetic rats, β2AR agonists inhibited diabetes-induced tumor necrosis factor-α production, which was prevented by co-treatment with a selective β2AR blocker...
July 2017: Kidney International
Ziwei Lin, Yu Zhao, Lige Song, Kaida Mu, Mingliang Zhang, Hongxia Liu, Xiaowen Li, Jian Zhao, Chen Wang, Weiping Jia
β-Arrestin2 (βarr2) is an adaptor protein that interacts with numerous signalling molecules and regulates insulin sensitivity. We reported previously that βarr2 was abundantly expressed in mouse pancreatic beta-cells, and loss of βarr2 leads to impairment of acute- and late-phase insulin secretion. In the present study, we examined the dynamic changes of beta-cell mass in βarr2-deficient (βarr2(-/-)) mice in vivo and explore the underlying mechanisms involved. βarr2(-/-) mice with luciferase exclusively overexpression in beta-cells were generated and fed with a high-fat diet (HFD)...
February 29, 2016: Molecular Medicine
Magalie A Ravier, Michele Leduc, Joy Richard, Nathalie Linck, Annie Varrault, Nelly Pirot, Morgane M Roussel, Joël Bockaert, Stéphane Dalle, Gyslaine Bertrand
AIMS/HYPOTHESIS: Beta cell failure due to progressive secretory dysfunction and limited expansion of beta cell mass is a key feature of type 2 diabetes. Beta cell function and mass are controlled by glucose and hormones/neurotransmitters that activate G protein-coupled receptors or receptor tyrosine kinases. We have investigated the role of β-arrestin (ARRB)2, a scaffold protein known to modulate such receptor signalling, in the modulation of beta cell function and mass, with a specific interest in glucagon-like peptide-1 (GLP-1), muscarinic and insulin receptors...
March 2014: Diabetologia
Dong-Ping Xie, Sen Li, Liang Li, Xin-Wen Chang, Tao-Fang Xi, Xiao Yang, Zhi Jin, Ying Zeng
Colonic dysmotility occurs in diabetes and the patients exhibit diarrhea or constipation. The pathogenetic mechanisms underlying colonic dysmotility in diabetic patients remain poorly understood. The effects of β-arrestin2 on colonic contraction in diabetic rats were investigated for the first time. Male SD rats were treated with a single intraperitoneally injected dose of streptozotocin, and those displaying sustained high blood glucose were selected as diabetes mellitus models. Longitudinal muscle strips of the distal colon were prepared to monitor contraction of the colon in vitro...
August 10, 2013: Regulatory Peptides
Mingliang Zhang, Yunxia Zhu, Kaida Mu, Ling Li, Junxi Lu, Jian Zhao, Xinyi Huang, Chen Wang, Weiping Jia
Insulin resistance and defective insulin secretion are two major factors contributing to the pathogenesis of type 2 diabetes. β-Arrestin2 is known to interact with numerous signaling molecules. Our previous study demonstrated that β-arrestin2 regulates insulin sensitivity in both skeletal muscle and liver, yet its role in insulin secretion remains elusive. In this study, we found that β-arrestin2 was abundantly expressed in mouse pancreatic beta cells, while its expression was significantly decreased in obese and diabetic mouse models...
June 7, 2013: Biochemical and Biophysical Research Communications
Ivo Quack, Magdalena Woznowski, Sebastian A Potthoff, Romy Palmer, Eva Königshausen, Sema Sivritas, Mario Schiffer, Johannes Stegbauer, Oliver Vonend, Lars Christian Rump, Lorenz Sellin
Nephrin, the key molecule of the glomerular slit diaphragm, is expressed on the surface of podocytes and is critical in preventing albuminuria. In diabetes, hyperglycemia leads to the loss of surface expression of nephrin and causes albuminuria. Here, we report a mechanism that can explain this phenomenon: hyperglycemia directly enhances the rate of nephrin endocytosis via regulation of the β-arrestin2-nephrin interaction by PKCα. We identified PKCα and protein interacting with c kinase-1 (PICK1) as nephrin-binding proteins...
April 15, 2011: Journal of Biological Chemistry
Lada Krilov, Amy Nguyen, Teruo Miyazaki, Cecilia G Unson, Bernard Bouscarel
Glucagon receptor (GR) activity and expression are altered in several diseases, including Type 2 diabetes. Previously, we investigated the mechanism of GR desensitization and internalization. The present study focused on the fate of internalized GR. Using both hamster hepatocytes and human embryonic kidney (HEK)-293 cells, we showed that internalized GR recycled to the plasma membrane within 30-60 min following stimulation of the cells with 100 nM glucagon. In HEK-293 cells and during recycling, GR colocalized with Rab4, Rab11, beta-arrestin1, beta-arrestin2, and actin filaments, in the cytosolic and/or perinuclear domains...
November 2008: American Journal of Physiology. Cell Physiology
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