Advanced glycation end‐products activate extracellular signal‐regulated kinase via the oxidative stress‐EGF receptor pathway in renal fibroblasts
作者： San-Cher Chen , Jinn-Yuh Guh , Chi-Ching Hwang , Shean-Jaw Chiou , Tai-Du Lin
DOI: 10.1002/JCB.22376
关键词: Protein phosphorylation 、 Endocrinology 、 Glycation 、 RAGE (receptor) 、 Molecular biology 、 Kidney metabolism 、 Internal medicine 、 Kinase 、 Reactive oxygen species 、 MAPK/ERK pathway 、 Receptor 、 Chemistry
摘要: Advanced glycation end-products (AGEs), epidermal growth factor receptor (EGFR), reactive oxygen species (ROS), and extracellular signal-regulated kinases (ERK) are implicated in diabetic nephropathy (DN). Therefore, we asked if AGEs-induced ERK protein phosphorylation mitogenesis dependent on the for AGEs (RAGE)-ROS-EGFR pathway normal rat kidney interstitial fibroblast (NRK-49F) cells. We found that (100 microg/ml) activated EGFR ERK1/2, which was attenuated by RAGE short-hairpin RNA (shRNA). also increased intracellular ROS levels while shRNA N-acetylcysteine (NAC) ROS. Hydrogen peroxide (5-25 microM) level activating both ERK1/2. Low-dose hydrogen (5 whereas high-dose decreased at 3 days. AGEs-activated ERK1/2 were an anti-oxidant inhibitor (Iressa). Moreover, shRNA, NAC, Iressa, (PD98059). In conclusion, it is RAGE-ROS-EGFR-ERK1/2 RAGE-ROS-EGFR NRK-49F
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