Deletion of scavenger receptor A protects mice from progressive nephropathy independent of lipid control during diet-induced hyperlipidemia
Scavenger receptor A (SR-A) is a key transmembrane receptor in the endocytosis of lipids and contributes to the pathogenesis of atherosclerosis. To assess its role in hyperlipidemic chronic kidney disease, wild-type and SR-A-deficient (knockout) mice underwent uninephrectomy followed by either norma...
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| Veröffentlicht in: | Kidney international 2012-05, Vol.81 (10), p.1002-1014 |
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| creator | Wang, Wenjian He, Bin Shi, Wei Liang, Xinling Ma, Jianchao Shan, Zhixin Hu, Zhaoyong Danesh, Farhad R. |
| description | Scavenger receptor A (SR-A) is a key transmembrane receptor in the endocytosis of lipids and contributes to the pathogenesis of atherosclerosis. To assess its role in hyperlipidemic chronic kidney disease, wild-type and SR-A-deficient (knockout) mice underwent uninephrectomy followed by either normal or high-fat diet. After 16 weeks of diet intervention, hyperlipidemic wild-type mice presented characteristic features of progressive nephropathy: albuminuria, renal fibrosis, and overexpression of transforming growth factor (TGF)-β1/Smad. These changes were markedly diminished in hyperlipidemic knockout mice and attributed to reduced renal lipid retention, oxidative stress, and CD11c+ cell infiltration. In vitro, overexpression of SR-A augmented monocyte chemoattractant protein-1 release and TGF-β1/Smad activation in HK-2 cells exposed to oxidized low-density lipoprotein. SR-A knockdown prevented lipid-induced cell injury. Moreover, wild-type to knockout bone marrow transplantation resulted in renal fibrosis in uninephrectomized mice following 16 weeks of the high-fat diet. In contrast, knockout to wild-type bone marrow transplantation led to markedly reduced albuminuria, CD11c+ cell infiltration, and renal fibrosis compared to wild-type to SR-A knockout or wild-type to wild-type bone marrow transplanted mice, without difference in plasma lipid levels. Thus, SR-A on circulating leukocytes rather than resident renal cells predominantly mediates lipid-induced kidney injury. |
| doi_str_mv | 10.1038/ki.2011.457 |
| format | Article |
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To assess its role in hyperlipidemic chronic kidney disease, wild-type and SR-A-deficient (knockout) mice underwent uninephrectomy followed by either normal or high-fat diet. After 16 weeks of diet intervention, hyperlipidemic wild-type mice presented characteristic features of progressive nephropathy: albuminuria, renal fibrosis, and overexpression of transforming growth factor (TGF)-β1/Smad. These changes were markedly diminished in hyperlipidemic knockout mice and attributed to reduced renal lipid retention, oxidative stress, and CD11c+ cell infiltration. In vitro, overexpression of SR-A augmented monocyte chemoattractant protein-1 release and TGF-β1/Smad activation in HK-2 cells exposed to oxidized low-density lipoprotein. SR-A knockdown prevented lipid-induced cell injury. Moreover, wild-type to knockout bone marrow transplantation resulted in renal fibrosis in uninephrectomized mice following 16 weeks of the high-fat diet. In contrast, knockout to wild-type bone marrow transplantation led to markedly reduced albuminuria, CD11c+ cell infiltration, and renal fibrosis compared to wild-type to SR-A knockout or wild-type to wild-type bone marrow transplanted mice, without difference in plasma lipid levels. Thus, SR-A on circulating leukocytes rather than resident renal cells predominantly mediates lipid-induced kidney injury.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1038/ki.2011.457</identifier><identifier>PMID: 22377830</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>Basingstoke: Elsevier Inc</publisher><subject>Albuminuria - etiology ; Albuminuria - metabolism ; Albuminuria - prevention & control ; Animals ; Biological and medical sciences ; Bone Marrow Transplantation ; CD11c Antigen - metabolism ; CD11c-positive cell ; Cell Line ; Chemokine CCL2 - metabolism ; Chronic Disease ; Dietary Fats - blood ; Dietary Fats - metabolism ; Disease Models, Animal ; Disease Progression ; Disorders of blood lipids. Hyperlipoproteinemia ; Fibrosis ; hyperlipidemia ; Hyperlipidemias - complications ; Hyperlipidemias - etiology ; Kidney - metabolism ; Kidney - pathology ; Kidney Diseases - etiology ; Kidney Diseases - genetics ; Kidney Diseases - metabolism ; Kidney Diseases - pathology ; Kidney Diseases - prevention & control ; Leukocytes - metabolism ; Male ; Medical sciences ; Metabolic diseases ; Mice ; Mice, Knockout ; Nephrectomy ; Nephrology. Urinary tract diseases ; Original ; Oxidative Stress ; RNA Interference ; scavenger receptor A ; Scavenger Receptors, Class A - deficiency ; Scavenger Receptors, Class A - genetics ; Scavenger Receptors, Class A - metabolism ; Signal Transduction ; Smad Proteins - metabolism ; Superoxide Dismutase - genetics ; Superoxide Dismutase - metabolism ; Time Factors ; Transfection ; Transforming Growth Factor beta1 - metabolism ; transforming growth factor-β1</subject><ispartof>Kidney international, 2012-05, Vol.81 (10), p.1002-1014</ispartof><rights>2012 International Society of Nephrology</rights><rights>2015 INIST-CNRS</rights><rights>Copyright Nature Publishing Group May 2012</rights><rights>Copyright © 2012 International Society of Nephrology 2012 International Society of Nephrology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c551t-5f0a4a2b2b67f65e12d76b0f35b8f121eb421b36402aeefb113e06e09bcf119e3</citedby><cites>FETCH-LOGICAL-c551t-5f0a4a2b2b67f65e12d76b0f35b8f121eb421b36402aeefb113e06e09bcf119e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1010246763?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>230,314,776,780,881,27903,27904,64362,64364,64366,72216</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25867799$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22377830$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Wenjian</creatorcontrib><creatorcontrib>He, Bin</creatorcontrib><creatorcontrib>Shi, Wei</creatorcontrib><creatorcontrib>Liang, Xinling</creatorcontrib><creatorcontrib>Ma, Jianchao</creatorcontrib><creatorcontrib>Shan, Zhixin</creatorcontrib><creatorcontrib>Hu, Zhaoyong</creatorcontrib><creatorcontrib>Danesh, Farhad R.</creatorcontrib><title>Deletion of scavenger receptor A protects mice from progressive nephropathy independent of lipid control during diet-induced hyperlipidemia</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Scavenger receptor A (SR-A) is a key transmembrane receptor in the endocytosis of lipids and contributes to the pathogenesis of atherosclerosis. To assess its role in hyperlipidemic chronic kidney disease, wild-type and SR-A-deficient (knockout) mice underwent uninephrectomy followed by either normal or high-fat diet. After 16 weeks of diet intervention, hyperlipidemic wild-type mice presented characteristic features of progressive nephropathy: albuminuria, renal fibrosis, and overexpression of transforming growth factor (TGF)-β1/Smad. These changes were markedly diminished in hyperlipidemic knockout mice and attributed to reduced renal lipid retention, oxidative stress, and CD11c+ cell infiltration. In vitro, overexpression of SR-A augmented monocyte chemoattractant protein-1 release and TGF-β1/Smad activation in HK-2 cells exposed to oxidized low-density lipoprotein. SR-A knockdown prevented lipid-induced cell injury. Moreover, wild-type to knockout bone marrow transplantation resulted in renal fibrosis in uninephrectomized mice following 16 weeks of the high-fat diet. In contrast, knockout to wild-type bone marrow transplantation led to markedly reduced albuminuria, CD11c+ cell infiltration, and renal fibrosis compared to wild-type to SR-A knockout or wild-type to wild-type bone marrow transplanted mice, without difference in plasma lipid levels. Thus, SR-A on circulating leukocytes rather than resident renal cells predominantly mediates lipid-induced kidney injury.</description><subject>Albuminuria - etiology</subject><subject>Albuminuria - metabolism</subject><subject>Albuminuria - prevention & control</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bone Marrow Transplantation</subject><subject>CD11c Antigen - metabolism</subject><subject>CD11c-positive cell</subject><subject>Cell Line</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Chronic Disease</subject><subject>Dietary Fats - blood</subject><subject>Dietary Fats - metabolism</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Disorders of blood lipids. Hyperlipoproteinemia</subject><subject>Fibrosis</subject><subject>hyperlipidemia</subject><subject>Hyperlipidemias - complications</subject><subject>Hyperlipidemias - etiology</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidney Diseases - etiology</subject><subject>Kidney Diseases - genetics</subject><subject>Kidney Diseases - metabolism</subject><subject>Kidney Diseases - pathology</subject><subject>Kidney Diseases - prevention & control</subject><subject>Leukocytes - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Nephrectomy</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Original</subject><subject>Oxidative Stress</subject><subject>RNA Interference</subject><subject>scavenger receptor A</subject><subject>Scavenger Receptors, Class A - deficiency</subject><subject>Scavenger Receptors, Class A - genetics</subject><subject>Scavenger Receptors, Class A - metabolism</subject><subject>Signal Transduction</subject><subject>Smad Proteins - metabolism</subject><subject>Superoxide Dismutase - genetics</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Time Factors</subject><subject>Transfection</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>transforming growth factor-β1</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkluL3CAYhqW0dKfbXvW-CKVQKJl6iDG5WVi2R1joTXstxnzOuJtoqmZgfkP_dJ2d6fZAbxT14eXVR4SeU7KmhLdvb92aEUrXtZAP0IoKxisqhXiIVoS0omKCt2foSUo3pKw7Th6jM8a4lC0nK_TjHYyQXfA4WJyM3oHfQMQRDMw5RHyJ5xgymJzw5AxgG8N02NpESMntAHuYtzHMOm_32PkBZiiDz4e40c1uwCb4HMOIhyU6v8GDg1wVcDEw4O1-hniHweT0U_TI6jHBs9N8jr59eP_16lN1_eXj56vL68oIQXMlLNG1Zj3rG2kbAZQNsumJ5aJvLWUU-prRnjc1YRrA9pRyIA2QrjeW0g74Obo45s5LP8FgSt2oRzVHN-m4V0E79feJd1u1CTvFec05rUvA61NADN8XSFlNLhkYR-0hLElRQkndCSJZQV_-g96EJfpyvTuK1Y1seKHeHCkTQ0oR7H0ZStRBsrp16iBZFcmFfvFn_3v2l9UCvDoBuigdbdTeuPSbE20jZdcVThw5KK-9cxBVMg58MePKB8hqCO6_BX4CytnFLA</recordid><startdate>20120501</startdate><enddate>20120501</enddate><creator>Wang, Wenjian</creator><creator>He, Bin</creator><creator>Shi, Wei</creator><creator>Liang, Xinling</creator><creator>Ma, Jianchao</creator><creator>Shan, Zhixin</creator><creator>Hu, Zhaoyong</creator><creator>Danesh, Farhad R.</creator><general>Elsevier Inc</general><general>Nature Publishing Group</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20120501</creationdate><title>Deletion of scavenger receptor A protects mice from progressive nephropathy independent of lipid control during diet-induced hyperlipidemia</title><author>Wang, Wenjian ; He, Bin ; Shi, Wei ; Liang, Xinling ; Ma, Jianchao ; Shan, Zhixin ; Hu, Zhaoyong ; Danesh, Farhad R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c551t-5f0a4a2b2b67f65e12d76b0f35b8f121eb421b36402aeefb113e06e09bcf119e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Albuminuria - etiology</topic><topic>Albuminuria - metabolism</topic><topic>Albuminuria - prevention & control</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bone Marrow Transplantation</topic><topic>CD11c Antigen - metabolism</topic><topic>CD11c-positive cell</topic><topic>Cell Line</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Chronic Disease</topic><topic>Dietary Fats - blood</topic><topic>Dietary Fats - metabolism</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>Disorders of blood lipids. Hyperlipoproteinemia</topic><topic>Fibrosis</topic><topic>hyperlipidemia</topic><topic>Hyperlipidemias - complications</topic><topic>Hyperlipidemias - etiology</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidney Diseases - etiology</topic><topic>Kidney Diseases - genetics</topic><topic>Kidney Diseases - metabolism</topic><topic>Kidney Diseases - pathology</topic><topic>Kidney Diseases - prevention & control</topic><topic>Leukocytes - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Nephrectomy</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Original</topic><topic>Oxidative Stress</topic><topic>RNA Interference</topic><topic>scavenger receptor A</topic><topic>Scavenger Receptors, Class A - deficiency</topic><topic>Scavenger Receptors, Class A - genetics</topic><topic>Scavenger Receptors, Class A - metabolism</topic><topic>Signal Transduction</topic><topic>Smad Proteins - metabolism</topic><topic>Superoxide Dismutase - genetics</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Time Factors</topic><topic>Transfection</topic><topic>Transforming Growth Factor beta1 - metabolism</topic><topic>transforming growth factor-β1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Wenjian</creatorcontrib><creatorcontrib>He, Bin</creatorcontrib><creatorcontrib>Shi, Wei</creatorcontrib><creatorcontrib>Liang, Xinling</creatorcontrib><creatorcontrib>Ma, Jianchao</creatorcontrib><creatorcontrib>Shan, Zhixin</creatorcontrib><creatorcontrib>Hu, Zhaoyong</creatorcontrib><creatorcontrib>Danesh, Farhad R.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Wenjian</au><au>He, Bin</au><au>Shi, Wei</au><au>Liang, Xinling</au><au>Ma, Jianchao</au><au>Shan, Zhixin</au><au>Hu, Zhaoyong</au><au>Danesh, Farhad R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deletion of scavenger receptor A protects mice from progressive nephropathy independent of lipid control during diet-induced hyperlipidemia</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2012-05-01</date><risdate>2012</risdate><volume>81</volume><issue>10</issue><spage>1002</spage><epage>1014</epage><pages>1002-1014</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Scavenger receptor A (SR-A) is a key transmembrane receptor in the endocytosis of lipids and contributes to the pathogenesis of atherosclerosis. To assess its role in hyperlipidemic chronic kidney disease, wild-type and SR-A-deficient (knockout) mice underwent uninephrectomy followed by either normal or high-fat diet. After 16 weeks of diet intervention, hyperlipidemic wild-type mice presented characteristic features of progressive nephropathy: albuminuria, renal fibrosis, and overexpression of transforming growth factor (TGF)-β1/Smad. These changes were markedly diminished in hyperlipidemic knockout mice and attributed to reduced renal lipid retention, oxidative stress, and CD11c+ cell infiltration. In vitro, overexpression of SR-A augmented monocyte chemoattractant protein-1 release and TGF-β1/Smad activation in HK-2 cells exposed to oxidized low-density lipoprotein. SR-A knockdown prevented lipid-induced cell injury. Moreover, wild-type to knockout bone marrow transplantation resulted in renal fibrosis in uninephrectomized mice following 16 weeks of the high-fat diet. In contrast, knockout to wild-type bone marrow transplantation led to markedly reduced albuminuria, CD11c+ cell infiltration, and renal fibrosis compared to wild-type to SR-A knockout or wild-type to wild-type bone marrow transplanted mice, without difference in plasma lipid levels. Thus, SR-A on circulating leukocytes rather than resident renal cells predominantly mediates lipid-induced kidney injury.</abstract><cop>Basingstoke</cop><pub>Elsevier Inc</pub><pmid>22377830</pmid><doi>10.1038/ki.2011.457</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; ProQuest Central UK/Ireland; Alma/SFX Local Collection |
| subjects | Albuminuria - etiology Albuminuria - metabolism Albuminuria - prevention & control Animals Biological and medical sciences Bone Marrow Transplantation CD11c Antigen - metabolism CD11c-positive cell Cell Line Chemokine CCL2 - metabolism Chronic Disease Dietary Fats - blood Dietary Fats - metabolism Disease Models, Animal Disease Progression Disorders of blood lipids. Hyperlipoproteinemia Fibrosis hyperlipidemia Hyperlipidemias - complications Hyperlipidemias - etiology Kidney - metabolism Kidney - pathology Kidney Diseases - etiology Kidney Diseases - genetics Kidney Diseases - metabolism Kidney Diseases - pathology Kidney Diseases - prevention & control Leukocytes - metabolism Male Medical sciences Metabolic diseases Mice Mice, Knockout Nephrectomy Nephrology. Urinary tract diseases Original Oxidative Stress RNA Interference scavenger receptor A Scavenger Receptors, Class A - deficiency Scavenger Receptors, Class A - genetics Scavenger Receptors, Class A - metabolism Signal Transduction Smad Proteins - metabolism Superoxide Dismutase - genetics Superoxide Dismutase - metabolism Time Factors Transfection Transforming Growth Factor beta1 - metabolism transforming growth factor-β1 |
| title | Deletion of scavenger receptor A protects mice from progressive nephropathy independent of lipid control during diet-induced hyperlipidemia |
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