The ACE2-Angiotensin-(1–7)-Mas Axis Protects Against Pancreatic Cell Damage in Cell Culture. Issue 2 (March 2015)

• Record Type: Journal Article
• Authors: Wang, Jing; Liu, Ruixia; Qi, Haiyu; Wang, Yan; Cui, Lijian; Wen, Yan; Li, Huihui; Yin, Chenghong
• Is Part Of: Pancreas. Volume 44:Issue 2(2015)
• Publication Date: 2015-03
• Subjects: ACE2 -- angiotensin-(1–7) -- Mas -- protection effect -- pancreatic cell damage; Pancreas -- Diseases -- Periodicals; Pancreas -- Periodicals; Neuroendocrine tumors -- Periodicals; 616.37005
• DOI: 10.1097/MPA.0000000000000247
• Languages: English
• ISSNs: 0885-3177

Abstract

Abstract : Objective: Angiotensin-converting enzyme 2 (ACE2), its product angiotensin-(1–7), and its receptor Mas have been shown to moderate the adverse effects of the ACE-angiotensin II-AT1 axis in many diseases. The aim of this study was to determine whether the ACE2-Ang-(1–7)-Mas axis could have similar effects in a cell culture model of pancreatic damage. Methods: AR42J cells were stimulated with 10 nmol/L cerulein to simulate acute pancreatitis. ACE2, Ang-(1–7), Mas receptor, and PI3K/AKT pathway were measured by quantitative real-time polymerase chain reaction and Western blot analysis. Results: ACE2 and Mas receptor protein levels in AR42J cells were significantly increased ( P < 0.05) between 30 minutes and 6 hours postdisease induction compared with the control group. Mas receptor gene expression was significantly increased ( P < 0.05) at 2 hours postdisease induction, and Ang-(1–7) was increased at 6 hours. Treatment with Ang-(1–7) in AR42J cells increased IL-10, decreased IL-6 and IL-8, and reduced the damage to pancreatic cells. Levels of IL-6 and IL-8 in AR42J cell culture were increased significantly after treatment with A779. Moreover, Ang-(1–7) increased the concentration of PI3K/AKT pathway and eNOSin AR42J cells. Conclusions: ACE2-angiotensin-(1–7)-Mas axis significantly inhibits pancreatitis in response to decreased inflammatory factors by the activation of endothelial nitric oxide synthase and NO signaling pathways.