RAGE does not contribute to renal injury and damage upon ischemia/reperfusion-induced injury.

Abstract

The receptor for advanced glycation end products (RAGE) mediates a variety of inflammatory responses in renal diseases, but its role in renal ischemia/reperfusion (I/R) injury is unknown. We showed that during renal I/R, RAGE ligands HMGB1 and S100B are expressed. However, RAGE deficiency does not affect renal injury and function upon I/R-induced injury.

• Authors: Mark C Dessing, Wilco P Pulskens, Gwendoline J Teske, Loes M Butter, Tom van der Poll, Huan Yang, Kevin J Tracey, Peter P Nawroth, Angelika Bierhaus, Sandrine Florquin, Jaklien C Leemans
• Journal: Journal of innate immunity (J Innate Immun) Vol. 4 Issue 1 Pg. 80-5 ( 2012) ISSN: 1662-8128 [Electronic] Switzerland
• PMID: 22067944 (Publication Type: Journal Article)
• Copyright: Copyright © 2011 S. Karger AG, Basel.

Chemical References

• HMGB1 Protein
• Nerve Growth Factors
• Receptor for Advanced Glycation End Products
• Receptors, Immunologic
• S100 Calcium Binding Protein beta Subunit
• S100 Proteins
• S100b protein, mouse

Topics

• Animals
• Bowman Capsule (immunology, metabolism, pathology)
• Gene Expression Regulation (genetics, immunology)
• HMGB1 Protein (biosynthesis, genetics, immunology)
• Kidney Diseases (genetics, immunology, metabolism, pathology)
• Kidney Tubules, Proximal (immunology, metabolism, pathology)
• Mice
• Mice, Knockout
• Nerve Growth Factors (biosynthesis, genetics, immunology)
• Podocytes (immunology, metabolism, pathology)
• Receptor for Advanced Glycation End Products
• Receptors, Immunologic (genetics, immunology, metabolism)
• Reperfusion Injury (genetics, immunology, metabolism, pathology)
• S100 Calcium Binding Protein beta Subunit
• S100 Proteins (biosynthesis, genetics, immunology)