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.
Copyright © 2011 S. Karger AG, Basel.
MeSH terms
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Animals
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Bowman Capsule / immunology*
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Bowman Capsule / metabolism
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Bowman Capsule / pathology
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Gene Expression Regulation / genetics
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Gene Expression Regulation / immunology
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HMGB1 Protein / biosynthesis
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HMGB1 Protein / genetics
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HMGB1 Protein / immunology
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Kidney Diseases / genetics
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Kidney Diseases / immunology*
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Kidney Diseases / metabolism
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Kidney Diseases / pathology
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Kidney Tubules, Proximal / immunology*
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Kidney Tubules, Proximal / metabolism
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Kidney Tubules, Proximal / pathology
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Mice
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Mice, Knockout
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Nerve Growth Factors / biosynthesis
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Nerve Growth Factors / genetics
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Nerve Growth Factors / immunology
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Podocytes / immunology*
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Podocytes / metabolism
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Podocytes / pathology
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Receptor for Advanced Glycation End Products
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Receptors, Immunologic / genetics
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Receptors, Immunologic / immunology*
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Receptors, Immunologic / metabolism
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Reperfusion Injury / genetics
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Reperfusion Injury / immunology*
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Reperfusion Injury / metabolism
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Reperfusion Injury / pathology
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S100 Calcium Binding Protein beta Subunit
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S100 Proteins / biosynthesis
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S100 Proteins / genetics
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S100 Proteins / immunology
Substances
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HMGB1 Protein
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Nerve Growth Factors
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Receptor for Advanced Glycation End Products
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Receptors, Immunologic
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S100 Calcium Binding Protein beta Subunit
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S100 Proteins
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S100b protein, mouse