Hydrogen Sulfide Prevents Advanced Glycation End-Products Induced Activation of the Epithelial Sodium Channel
| Autor: | Chen Liang, Bin-Lin Song, He-Ping Ma, Shuai Jiang, Dan Zhao, Jing Shi, Xin-Yuan Li, Qiu-Shi Wang, Ying-Ying Sun, Xiao Chen, Zhi-Ren Zhang, Ming-Ming Wu |
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| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
Glycation End Products
Advanced Epithelial sodium channel Aging medicine.medical_specialty Patch-Clamp Techniques Article Subject Morpholines Xenopus Sodium chemistry.chemical_element Sulfides Xenopus Proteins Biochemistry Cell Line Cyclic N-Oxides Phosphatidylinositol 3-Kinases chemistry.chemical_compound Glycation Internal medicine medicine Animals LY294002 lcsh:QH573-671 Epithelial Sodium Channels PI3K/AKT/mTOR pathway Amitrole Phosphoinositide-3 Kinase Inhibitors Microscopy Confocal Renal sodium reabsorption biology urogenital system lcsh:Cytology PTEN Phosphohydrolase Nephrons Cell Biology General Medicine respiratory system Catalase Oxidative Stress Endocrinology chemistry Chromones biology.protein Spin Labels Reactive Oxygen Species Homeostasis Research Article Signal Transduction |
| Zdroj: | Oxidative Medicine and Cellular Longevity, Vol 2015 (2015) Oxidative Medicine and Cellular Longevity |
| ISSN: | 1942-0994 1942-0900 |
| Popis: | Advanced glycation end-products (AGEs) are complex and heterogeneous compounds implicated in diabetes. Sodium reabsorption through the epithelial sodium channel (ENaC) at the distal nephron plays an important role in diabetic hypertension. Here, we report that H2S antagonizes AGEs-induced ENaC activation in A6 cells. ENaC open probability(PO)in A6 cells was significantly increased by exogenous AGEs and that this AGEs-induced ENaC activity was abolished by NaHS (a donor of H2S) and TEMPOL. Incubating A6 cells with the catalase inhibitor 3-aminotriazole (3-AT) mimicked the effects of AGEs on ENaC activity, but did not induce any additive effect. We found that the expression levels of catalase were significantly reduced by AGEs and both AGEs and 3-AT facilitated ROS uptake in A6 cells, which were significantly inhibited by NaHS. The specific PTEN and PI3K inhibitors, BPV(pic) and LY294002, influence ENaC activity in AGEs-pretreated A6 cells. Moreover, after removal of AGEs from AGEs-pretreated A6 cells for 72 hours, ENaCPOremained at a high level, suggesting that an AGEs-related “metabolic memory” may be involved in sodium homeostasis. Our data, for the first time, show that H2S prevents AGEs-induced ENaC activation by targeting the ROS/PI3K/PTEN pathway. |
| Databáze: | OpenAIRE |
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