A2a adenosine receptor agonist improves endoplasmic reticulum stress in MIN6 cell line through protein kinase A/ protein kinase B/ Cyclic adenosine monophosphate response element ‐binding protein/ and Growth Arrest And DNA‐Damage‐Inducible 34/ eukaryotic Initiation Factor 2α pathways

A2a adenosine receptor activation improved endoplasmic reticulum (ER) stress in pancreatic beta cells (PBCs) and its signaling may provide new approach to control ER stress in the PBC cells. AbstractEndoplasmic reticulum (ER) stress is one of the main molecular events underlying pancreatic beta cell (PBC) failure, apoptosis, and a decrease in insulin secretion. Recent studies have highlighted the fundamental role of A2a adenosine receptor (A2aR) in potentiation of insulin secretion and proliferation of PBCs. However, possible protective effects of A2aR signaling against ER stress have not been elucidated yet. Thus, in the present study, we aimed to investigate the effects of A2aR activation in MIN6 beta cells undergoing tunicamycin (TM) ‐mediated ER stress. A2aR expression and activity were evaluated using real‐time polymerase chain reaction and measurement of the cyclic adenosine monophosphate (cAMP), protein kinase A (PKA), phospho‐protein kinase B or Akt (p‐Akt)/Akt, and phospho‐Cyclic adenosine monophosphate response element‐binding protein/CREB levels in response to a specific agonist (CGS 21680). Survival and proliferation in TM and CGS 21680 cotreated cells were evaluated using 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT), annexin V–fluorescein isothiocyanate (FITC)/propi dium iodide staining, colony formation, and 5‐bromo‐2′‐deoxyuridine (Brdu) assays. In addition, the effects of A2aR stimulation on insulin secre...
Source: Journal of Cellular Physiology - Category: Cytology Authors: Tags: ORIGINAL RESEARCH ARTICLE Source Type: research