Receptor of advanced glycation end products (RAGE) positively regulates CD36 expression and reactive oxygen species production in human monocytes in diabetes
Autor: | George Koliakos, Andreas Xanthis, Christina Befani, Apostolos I. Hatzitolios, Georgios Giannakoulas, S. Fidani |
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Rok vydání: | 2009 |
Předmět: |
CD36 Antigens
Glycation End Products Advanced Male medicine.medical_specialty endocrine system diseases CD36 Receptor for Advanced Glycation End Products Angiotensin-Converting Enzyme Inhibitors Monocytes RAGE (receptor) Glycation Internal medicine parasitic diseases Medicine Humans RNA Small Interfering Receptors Immunologic Receptor Aged chemistry.chemical_classification Gene knockdown Reactive oxygen species biology business.industry Monocyte Middle Aged medicine.anatomical_structure Endocrinology Spectrometry Fluorescence chemistry Diabetes Mellitus Type 2 Gene Expression Regulation biology.protein Female Cardiology and Cardiovascular Medicine business Reactive Oxygen Species Intracellular |
Zdroj: | Scopus-Elsevier |
ISSN: | 1940-1574 |
Popis: | Introduction: Advanced glycation end products (AGEs) engagement of a monocyte surface receptor (RAGE) induces atherosclerosis. AGEs also act as CD36 ligands. We studied reactive oxygen species (ROS) and CD36 expression after siRNA inhibition of RAGE expression in human monocytes. Methods: We isolated monocytes from: a) 10 type 2 diabetics, and b) 5 age- and sex-matched healthy individuals. CD36 expression and ROS production were evaluated before and after RAGE knockdown. Results: After incubation of monocytes with AGE + bovine serum albumin (BSA), CD36 expression and intracellular ROS increased significantly in all groups. In RAGE-knockdown monocytes, AGE-induced CD36 expression and ROS generation were also significantly inhibited. Conclusions: Blocking RAGE expression using siRNA in human monocytes led to a significant inhibition of CD36 expression and ROS production, suggesting a positive interaction between RAGE, CD36 expression and ROS generation in monocytes. |
Databáze: | OpenAIRE |
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