Angiotensin-(1-7) abolishes AGE-induced cellular hypertrophy and myofibroblast transformation via inhibition of ERK1/2
| Autor: | Mark C. Chappell, Ebaa M. Alzayadneh |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Glycation End Products
Advanced medicine.medical_specialty medicine.drug_class Biology Article Transforming Growth Factor beta Internal medicine Albumins Renin–angiotensin system medicine Animals Phosphorylation Receptor Extracellular Signal-Regulated MAP Kinases Myofibroblasts Kidney Antagonist Epithelial Cells Cell Biology Transforming growth factor beta Hypertrophy Receptor antagonist Peptide Fragments Rats Enzyme Activation medicine.anatomical_structure Losartan Endocrinology biology.protein cardiovascular system Angiotensin I Myofibroblast hormones hormone substitutes and hormone antagonists medicine.drug |
| Zdroj: | Cellular signalling. 26(12) |
| ISSN: | 1873-3913 |
| Popis: | Angiotensin-(1-7) (Ang-(1-7)/AT7-Mas receptor axis is an alternative pathway within the renin angiotensin system (RAS) that generally opposes the actions of Ang II/AT1 receptor pathway. Advanced glycated end product (AGEs) including glucose- and methylglyoxal-modified albumin (MGA) may contribute to the development and progression of diabetic nephropathy in part through activation of the Ang II/AT1 receptor system; however, the influence of AGE on the Ang-(1-7) arm of the RAS within the kidney is unclear. The present study assessed the impact of AGE on the Ang-(1-7) axis in NRK-52E renal epithelial cells. MGA exposure for 48 hours significantly reduced the intracellular levels of Ang-(1-7) approximately 50%; however, Ang I or Ang II expression was not altered. The reduced cellular content of Ang-(1-7) was associated with increased metabolism of the peptide to the inactive metabolite Ang-(1-4) [MGA: 175 ± 9 vs. Control: 115 ± 11 fmol/min/mg protein, p |
| Databáze: | OpenAIRE |
| Externí odkaz: |
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