Advanced Oxidation Protein Products Promote Inflammation in Diabetic Kidney through Activation of Renal Nicotinamide Adenine Dinucleotide Phosphate Oxidase
The involvement of inflammatory processes has been recognized in development and/or progression of diabetic nephropathy. However, the mechanisms involved in the pathogenesis of renal inflammation have not been completely understood. In this study, we tested the hypothesis that accumulation of advanc...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2008-04, Vol.149 (4), p.1829-1839 |
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| creator | Shi, Xiao Yun Hou, Fan Fan Niu, Hong Xin Wang, Guo Bao Xie, Di Guo, Zhi Jian Zhou, Zhan Mei Yang, Fang Tian, Jian Wei Zhang, Xun |
| description | The involvement of inflammatory processes has been recognized in development and/or progression of diabetic nephropathy. However, the mechanisms involved in the pathogenesis of renal inflammation have not been completely understood. In this study, we tested the hypothesis that accumulation of advanced oxidation protein products (AOPPs), which occurs in diabetes, may promote inflammatory responses in diabetic kidney. Streptozotocin-induced diabetic rats were randomized to iv injection of vehicle, native rat serum albumin (RSA), and AOPPs-modified RSA (AOPPs-RSA) in the presence or absence of oral administration of apocynin. A control group was followed concurrently. Compared with RSA- or vehicle-treated diabetic rats, AOPPs-RSA-treated animals displayed significant increase in renal macrophage infiltration and overexpression of monocyte chemoattractant protein-1 and TGF-β1. This was associated with deteriorated structural and functional abnormalities of diabetic kidney, such as glomerular hypertrophy, fibronectin accumulation, and albuminuria. AOPP challenge significantly increased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-dependent superoxide generation in renal homogenates and up-regulated membrane expression of renal NADPH oxidase subunits p47phox and gp91phox. All these AOPPs-induced perturbations in diabetic kidney could be prevented by the NADPH oxidase inhibitor apocynin. These data suggest that chronic accumulation of AOPPs may promote renal inflammation in diabetes probably through activation of renal NADPH oxidase. |
| doi_str_mv | 10.1210/en.2007-1544 |
| format | Article |
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However, the mechanisms involved in the pathogenesis of renal inflammation have not been completely understood. In this study, we tested the hypothesis that accumulation of advanced oxidation protein products (AOPPs), which occurs in diabetes, may promote inflammatory responses in diabetic kidney. Streptozotocin-induced diabetic rats were randomized to iv injection of vehicle, native rat serum albumin (RSA), and AOPPs-modified RSA (AOPPs-RSA) in the presence or absence of oral administration of apocynin. A control group was followed concurrently. Compared with RSA- or vehicle-treated diabetic rats, AOPPs-RSA-treated animals displayed significant increase in renal macrophage infiltration and overexpression of monocyte chemoattractant protein-1 and TGF-β1. This was associated with deteriorated structural and functional abnormalities of diabetic kidney, such as glomerular hypertrophy, fibronectin accumulation, and albuminuria. AOPP challenge significantly increased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-dependent superoxide generation in renal homogenates and up-regulated membrane expression of renal NADPH oxidase subunits p47phox and gp91phox. All these AOPPs-induced perturbations in diabetic kidney could be prevented by the NADPH oxidase inhibitor apocynin. These data suggest that chronic accumulation of AOPPs may promote renal inflammation in diabetes probably through activation of renal NADPH oxidase.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2007-1544</identifier><identifier>PMID: 18174276</identifier><identifier>CODEN: ENDOAO</identifier><language>eng</language><publisher>Bethesda, MD: Endocrine Society</publisher><subject>Abnormalities ; Accumulation ; Adenine ; Animals ; Biological and medical sciences ; Chemokine CCL2 - genetics ; Diabetes ; Diabetes mellitus ; Diabetes. Impaired glucose tolerance ; Diabetic Nephropathies - etiology ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Enzyme Activation ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Fibronectin ; Fundamental and applied biological sciences. Psychology ; Hypertrophy ; Inflammation ; Kidney - metabolism ; Kidney - pathology ; Kidneys ; Macrophages ; Male ; Medical sciences ; Monocyte chemoattractant protein ; Monocyte chemoattractant protein 1 ; Monocytes ; NAD(P)H oxidase ; NADPH Oxidases - physiology ; NADPH-diaphorase ; Nephritis - etiology ; Nephropathy ; Nicotinamide ; Nicotinamide adenine dinucleotide ; Oral administration ; Oxidase ; Oxidation ; Oxidation-Reduction ; Pathogenesis ; Proteins ; Proteins - metabolism ; Rats ; Rats, Sprague-Dawley ; Serum albumin ; Streptozocin ; Structure-function relationships ; Transforming Growth Factor beta1 - genetics ; Transforming growth factor-b1 ; Vertebrates: endocrinology</subject><ispartof>Endocrinology (Philadelphia), 2008-04, Vol.149 (4), p.1829-1839</ispartof><rights>Copyright © 2008 by the Endocrine Society 2008</rights><rights>2008 INIST-CNRS</rights><rights>Copyright © 2008 by the Endocrine Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c527t-99f90c2e84b21702ea966e64e4b9157761317db8c504042720f823a931b5262e3</citedby><cites>FETCH-LOGICAL-c527t-99f90c2e84b21702ea966e64e4b9157761317db8c504042720f823a931b5262e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27926,27927</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20193218$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18174276$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shi, Xiao Yun</creatorcontrib><creatorcontrib>Hou, Fan Fan</creatorcontrib><creatorcontrib>Niu, Hong Xin</creatorcontrib><creatorcontrib>Wang, Guo Bao</creatorcontrib><creatorcontrib>Xie, Di</creatorcontrib><creatorcontrib>Guo, Zhi Jian</creatorcontrib><creatorcontrib>Zhou, Zhan Mei</creatorcontrib><creatorcontrib>Yang, Fang</creatorcontrib><creatorcontrib>Tian, Jian Wei</creatorcontrib><creatorcontrib>Zhang, Xun</creatorcontrib><title>Advanced Oxidation Protein Products Promote Inflammation in Diabetic Kidney through Activation of Renal Nicotinamide Adenine Dinucleotide Phosphate Oxidase</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>The involvement of inflammatory processes has been recognized in development and/or progression of diabetic nephropathy. However, the mechanisms involved in the pathogenesis of renal inflammation have not been completely understood. In this study, we tested the hypothesis that accumulation of advanced oxidation protein products (AOPPs), which occurs in diabetes, may promote inflammatory responses in diabetic kidney. Streptozotocin-induced diabetic rats were randomized to iv injection of vehicle, native rat serum albumin (RSA), and AOPPs-modified RSA (AOPPs-RSA) in the presence or absence of oral administration of apocynin. A control group was followed concurrently. Compared with RSA- or vehicle-treated diabetic rats, AOPPs-RSA-treated animals displayed significant increase in renal macrophage infiltration and overexpression of monocyte chemoattractant protein-1 and TGF-β1. This was associated with deteriorated structural and functional abnormalities of diabetic kidney, such as glomerular hypertrophy, fibronectin accumulation, and albuminuria. AOPP challenge significantly increased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-dependent superoxide generation in renal homogenates and up-regulated membrane expression of renal NADPH oxidase subunits p47phox and gp91phox. All these AOPPs-induced perturbations in diabetic kidney could be prevented by the NADPH oxidase inhibitor apocynin. These data suggest that chronic accumulation of AOPPs may promote renal inflammation in diabetes probably through activation of renal NADPH oxidase.</description><subject>Abnormalities</subject><subject>Accumulation</subject><subject>Adenine</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Chemokine CCL2 - genetics</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Diabetic Nephropathies - etiology</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Enzyme Activation</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Fibronectin</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hypertrophy</subject><subject>Inflammation</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidneys</subject><subject>Macrophages</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Monocyte chemoattractant protein</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Monocytes</subject><subject>NAD(P)H oxidase</subject><subject>NADPH Oxidases - physiology</subject><subject>NADPH-diaphorase</subject><subject>Nephritis - etiology</subject><subject>Nephropathy</subject><subject>Nicotinamide</subject><subject>Nicotinamide adenine dinucleotide</subject><subject>Oral administration</subject><subject>Oxidase</subject><subject>Oxidation</subject><subject>Oxidation-Reduction</subject><subject>Pathogenesis</subject><subject>Proteins</subject><subject>Proteins - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Serum albumin</subject><subject>Streptozocin</subject><subject>Structure-function relationships</subject><subject>Transforming Growth Factor beta1 - genetics</subject><subject>Transforming growth factor-b1</subject><subject>Vertebrates: endocrinology</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10ctu1DAUBmALgehQ2LFGlhCwIcW3xPFyVChUVLRCsI4c-4RxldjBTir6LLxsPZOISghWvn06x0c_Qs8pOaGMknfgTxghsqClEA_QhipRFpJK8hBtCKG8kIzJI_Qkpet8FELwx-iI1lQKJqsN-r21N9obsPjyl7N6csHjqxgmcIfVzmZK-82Qr_C573o9DIvK4L3TLUzO4M_OerjF0y6G-ccOb83kbhYVOvwVvO7xF2fC5LwenAW8teCdh1zAz6aH_JAvr3YhjTud-xy-kuApetTpPsGzdT1G388-fDv9VFxcfjw_3V4UpmRyKpTqFDEMatGyPDcDraoKKgGiVbSUsqKcStvWpiSC5KkZ6WrGteK0LVnFgB-j10vdMYafM6SpGVwy0PfaQ5hTI4mgpSp5hi__gtdhjnm61HDKSakoOai3izIxpBSha8boBh1vG0qafWQN-GYfWbOPLPMXa9G5HcDe4zWjDF6tQCej-y7mvFz64xihijNaZ_dmcWEe_9eyWFvyRYK3wcScxBghpftp_vnRO6Eiu_g</recordid><startdate>20080401</startdate><enddate>20080401</enddate><creator>Shi, Xiao Yun</creator><creator>Hou, Fan Fan</creator><creator>Niu, Hong Xin</creator><creator>Wang, Guo Bao</creator><creator>Xie, Di</creator><creator>Guo, Zhi Jian</creator><creator>Zhou, Zhan Mei</creator><creator>Yang, Fang</creator><creator>Tian, Jian Wei</creator><creator>Zhang, Xun</creator><general>Endocrine Society</general><general>Oxford University Press</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20080401</creationdate><title>Advanced Oxidation Protein Products Promote Inflammation in Diabetic Kidney through Activation of Renal Nicotinamide Adenine Dinucleotide Phosphate Oxidase</title><author>Shi, Xiao Yun ; Hou, Fan Fan ; Niu, Hong Xin ; Wang, Guo Bao ; Xie, Di ; Guo, Zhi Jian ; Zhou, Zhan Mei ; Yang, Fang ; Tian, Jian Wei ; Zhang, Xun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c527t-99f90c2e84b21702ea966e64e4b9157761317db8c504042720f823a931b5262e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Abnormalities</topic><topic>Accumulation</topic><topic>Adenine</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Chemokine CCL2 - genetics</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Diabetic Nephropathies - etiology</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Enzyme Activation</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Fibronectin</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hypertrophy</topic><topic>Inflammation</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidneys</topic><topic>Macrophages</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Monocyte chemoattractant protein</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Monocytes</topic><topic>NAD(P)H oxidase</topic><topic>NADPH Oxidases - physiology</topic><topic>NADPH-diaphorase</topic><topic>Nephritis - etiology</topic><topic>Nephropathy</topic><topic>Nicotinamide</topic><topic>Nicotinamide adenine dinucleotide</topic><topic>Oral administration</topic><topic>Oxidase</topic><topic>Oxidation</topic><topic>Oxidation-Reduction</topic><topic>Pathogenesis</topic><topic>Proteins</topic><topic>Proteins - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Serum albumin</topic><topic>Streptozocin</topic><topic>Structure-function relationships</topic><topic>Transforming Growth Factor beta1 - genetics</topic><topic>Transforming growth factor-b1</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shi, Xiao Yun</creatorcontrib><creatorcontrib>Hou, Fan Fan</creatorcontrib><creatorcontrib>Niu, Hong Xin</creatorcontrib><creatorcontrib>Wang, Guo Bao</creatorcontrib><creatorcontrib>Xie, Di</creatorcontrib><creatorcontrib>Guo, Zhi Jian</creatorcontrib><creatorcontrib>Zhou, Zhan Mei</creatorcontrib><creatorcontrib>Yang, Fang</creatorcontrib><creatorcontrib>Tian, Jian Wei</creatorcontrib><creatorcontrib>Zhang, Xun</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shi, Xiao Yun</au><au>Hou, Fan Fan</au><au>Niu, Hong Xin</au><au>Wang, Guo Bao</au><au>Xie, Di</au><au>Guo, Zhi Jian</au><au>Zhou, Zhan Mei</au><au>Yang, Fang</au><au>Tian, Jian Wei</au><au>Zhang, Xun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Advanced Oxidation Protein Products Promote Inflammation in Diabetic Kidney through Activation of Renal Nicotinamide Adenine Dinucleotide Phosphate Oxidase</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2008-04-01</date><risdate>2008</risdate><volume>149</volume><issue>4</issue><spage>1829</spage><epage>1839</epage><pages>1829-1839</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><coden>ENDOAO</coden><abstract>The involvement of inflammatory processes has been recognized in development and/or progression of diabetic nephropathy. However, the mechanisms involved in the pathogenesis of renal inflammation have not been completely understood. In this study, we tested the hypothesis that accumulation of advanced oxidation protein products (AOPPs), which occurs in diabetes, may promote inflammatory responses in diabetic kidney. Streptozotocin-induced diabetic rats were randomized to iv injection of vehicle, native rat serum albumin (RSA), and AOPPs-modified RSA (AOPPs-RSA) in the presence or absence of oral administration of apocynin. A control group was followed concurrently. Compared with RSA- or vehicle-treated diabetic rats, AOPPs-RSA-treated animals displayed significant increase in renal macrophage infiltration and overexpression of monocyte chemoattractant protein-1 and TGF-β1. This was associated with deteriorated structural and functional abnormalities of diabetic kidney, such as glomerular hypertrophy, fibronectin accumulation, and albuminuria. AOPP challenge significantly increased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-dependent superoxide generation in renal homogenates and up-regulated membrane expression of renal NADPH oxidase subunits p47phox and gp91phox. All these AOPPs-induced perturbations in diabetic kidney could be prevented by the NADPH oxidase inhibitor apocynin. These data suggest that chronic accumulation of AOPPs may promote renal inflammation in diabetes probably through activation of renal NADPH oxidase.</abstract><cop>Bethesda, MD</cop><pub>Endocrine Society</pub><pmid>18174276</pmid><doi>10.1210/en.2007-1544</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Abnormalities Accumulation Adenine Animals Biological and medical sciences Chemokine CCL2 - genetics Diabetes Diabetes mellitus Diabetes. Impaired glucose tolerance Diabetic Nephropathies - etiology Endocrine pancreas. Apud cells (diseases) Endocrinopathies Enzyme Activation Etiopathogenesis. Screening. Investigations. Target tissue resistance Fibronectin Fundamental and applied biological sciences. Psychology Hypertrophy Inflammation Kidney - metabolism Kidney - pathology Kidneys Macrophages Male Medical sciences Monocyte chemoattractant protein Monocyte chemoattractant protein 1 Monocytes NAD(P)H oxidase NADPH Oxidases - physiology NADPH-diaphorase Nephritis - etiology Nephropathy Nicotinamide Nicotinamide adenine dinucleotide Oral administration Oxidase Oxidation Oxidation-Reduction Pathogenesis Proteins Proteins - metabolism Rats Rats, Sprague-Dawley Serum albumin Streptozocin Structure-function relationships Transforming Growth Factor beta1 - genetics Transforming growth factor-b1 Vertebrates: endocrinology |
| title | Advanced Oxidation Protein Products Promote Inflammation in Diabetic Kidney through Activation of Renal Nicotinamide Adenine Dinucleotide Phosphate Oxidase |
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