Expression and localization of PDGF-B, PDGF-D, and PDGF receptor in the kidney of angiotensin II-infused rat
Lipid accumulation in the kidney is a marker of tissue damage and may play a role in the development of renal injury. We have previously shown that long-term administration of angiotensin II in rats causes increased expression of transforming growth factor-β1, coupled with an accumulation of lipids...
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| Veröffentlicht in: | Laboratory investigation 2006-12, Vol.86 (12), p.1285-1292 |
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| creator | Ishizaka, Nobukazu Matsuzaki, Gen Saito, Kan Noiri, Eisei Mori, Ichiro Nagai, Ryozo |
| description | Lipid accumulation in the kidney is a marker of tissue damage and may play a role in the development of renal injury. We have previously shown that long-term administration of angiotensin II in rats causes increased expression of transforming growth factor-β1, coupled with an accumulation of lipids in the tubular and vascular wall cells in the kidney. In this study, we examine the regulation of expression of platelet-derived growth factor (PDGF) and its receptor system and their co-localization with lipid deposits in the kidneys of angiotensin II-infused rats. Real-time RT-PCR showed that expression of PDGF-B, PDGF-D, and PDGF receptor-β (PDGFR-β) mRNA was increased by angiotensin II infusion, and in situ hybridization showed the co-localization of these mRNAs. Tubular cells that had increased PDGF-B mRNA expression were positive for lipid deposition and also for cellular proliferation, which was indicated by the presence of proliferating cell nuclear antigen. By contrast, in the kidneys of angiotensin II-infused rats, apoptosis occurred in tubular cells that contained deposits of iron but not lipids. The deposition of lipids and upregulation of PDGF-B, PDGF-D, and PDGFR-β induced by administration of angiotensin II were all suppressed by the selective angiotensin II type 1 (AT1) receptor antagonist losartan, but not by the nonspecific vasodilator hydralazine. The findings that lipid accumulation, upregulation of PDGF-B, PDGF-D, and PDGFR-β, and cellular proliferation were topologically associated and regulated in an AT1 receptor-dependent manner in the kidney of angiotensin II-infused rats suggests that these phenomena are related. |
| doi_str_mv | 10.1038/labinvest.3700486 |
| format | Article |
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We have previously shown that long-term administration of angiotensin II in rats causes increased expression of transforming growth factor-β1, coupled with an accumulation of lipids in the tubular and vascular wall cells in the kidney. In this study, we examine the regulation of expression of platelet-derived growth factor (PDGF) and its receptor system and their co-localization with lipid deposits in the kidneys of angiotensin II-infused rats. Real-time RT-PCR showed that expression of PDGF-B, PDGF-D, and PDGF receptor-β (PDGFR-β) mRNA was increased by angiotensin II infusion, and in situ hybridization showed the co-localization of these mRNAs. Tubular cells that had increased PDGF-B mRNA expression were positive for lipid deposition and also for cellular proliferation, which was indicated by the presence of proliferating cell nuclear antigen. By contrast, in the kidneys of angiotensin II-infused rats, apoptosis occurred in tubular cells that contained deposits of iron but not lipids. The deposition of lipids and upregulation of PDGF-B, PDGF-D, and PDGFR-β induced by administration of angiotensin II were all suppressed by the selective angiotensin II type 1 (AT1) receptor antagonist losartan, but not by the nonspecific vasodilator hydralazine. The findings that lipid accumulation, upregulation of PDGF-B, PDGF-D, and PDGFR-β, and cellular proliferation were topologically associated and regulated in an AT1 receptor-dependent manner in the kidney of angiotensin II-infused rats suggests that these phenomena are related.</description><identifier>ISSN: 0023-6837</identifier><identifier>EISSN: 1530-0307</identifier><identifier>DOI: 10.1038/labinvest.3700486</identifier><identifier>PMID: 17043664</identifier><identifier>CODEN: LAINAW</identifier><language>eng</language><publisher>New York: Elsevier Inc</publisher><subject>angiotensin II ; Angiotensin II - pharmacology ; Angiotensin II - physiology ; Animals ; Antihypertensive Agents - pharmacology ; apoptosis ; Apoptosis - physiology ; Biological and medical sciences ; Biotechnology ; Cell Proliferation ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation - drug effects ; Hydralazine - pharmacology ; hypertension ; In Situ Hybridization ; Investigative techniques, diagnostic techniques (general aspects) ; Iron - metabolism ; Kidney - metabolism ; Kidney - physiology ; Laboratory Medicine ; lipid accumulation ; Lipid Metabolism - drug effects ; Lipid Metabolism - genetics ; Lipid Metabolism - physiology ; Losartan - pharmacology ; Lymphokines - metabolism ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Norepinephrine - pharmacology ; Pathology ; platelet-derived growth factor ; Platelet-Derived Growth Factor - metabolism ; Proto-Oncogene Proteins c-sis - metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor, Platelet-Derived Growth Factor beta - metabolism ; research-article ; RNA, Messenger - metabolism ; Vasoconstrictor Agents - pharmacology</subject><ispartof>Laboratory investigation, 2006-12, Vol.86 (12), p.1285-1292</ispartof><rights>2006 United States & Canadian Academy of Pathology</rights><rights>United States and Canadian Academy of Pathology, Inc. 2006</rights><rights>2007 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Dec 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c560t-c99eac8d68e385410b90499461fe1c87fdbee313ce6d5c06bc5559950c233cfa3</citedby><cites>FETCH-LOGICAL-c560t-c99eac8d68e385410b90499461fe1c87fdbee313ce6d5c06bc5559950c233cfa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18334033$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17043664$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ishizaka, Nobukazu</creatorcontrib><creatorcontrib>Matsuzaki, Gen</creatorcontrib><creatorcontrib>Saito, Kan</creatorcontrib><creatorcontrib>Noiri, Eisei</creatorcontrib><creatorcontrib>Mori, Ichiro</creatorcontrib><creatorcontrib>Nagai, Ryozo</creatorcontrib><title>Expression and localization of PDGF-B, PDGF-D, and PDGF receptor in the kidney of angiotensin II-infused rat</title><title>Laboratory investigation</title><addtitle>Lab Invest</addtitle><addtitle>Lab Invest</addtitle><description>Lipid accumulation in the kidney is a marker of tissue damage and may play a role in the development of renal injury. We have previously shown that long-term administration of angiotensin II in rats causes increased expression of transforming growth factor-β1, coupled with an accumulation of lipids in the tubular and vascular wall cells in the kidney. In this study, we examine the regulation of expression of platelet-derived growth factor (PDGF) and its receptor system and their co-localization with lipid deposits in the kidneys of angiotensin II-infused rats. Real-time RT-PCR showed that expression of PDGF-B, PDGF-D, and PDGF receptor-β (PDGFR-β) mRNA was increased by angiotensin II infusion, and in situ hybridization showed the co-localization of these mRNAs. Tubular cells that had increased PDGF-B mRNA expression were positive for lipid deposition and also for cellular proliferation, which was indicated by the presence of proliferating cell nuclear antigen. By contrast, in the kidneys of angiotensin II-infused rats, apoptosis occurred in tubular cells that contained deposits of iron but not lipids. The deposition of lipids and upregulation of PDGF-B, PDGF-D, and PDGFR-β induced by administration of angiotensin II were all suppressed by the selective angiotensin II type 1 (AT1) receptor antagonist losartan, but not by the nonspecific vasodilator hydralazine. The findings that lipid accumulation, upregulation of PDGF-B, PDGF-D, and PDGFR-β, and cellular proliferation were topologically associated and regulated in an AT1 receptor-dependent manner in the kidney of angiotensin II-infused rats suggests that these phenomena are related.</description><subject>angiotensin II</subject><subject>Angiotensin II - pharmacology</subject><subject>Angiotensin II - physiology</subject><subject>Animals</subject><subject>Antihypertensive Agents - pharmacology</subject><subject>apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>Biotechnology</subject><subject>Cell Proliferation</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Hydralazine - pharmacology</subject><subject>hypertension</subject><subject>In Situ Hybridization</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Iron - metabolism</subject><subject>Kidney - metabolism</subject><subject>Kidney - physiology</subject><subject>Laboratory Medicine</subject><subject>lipid accumulation</subject><subject>Lipid Metabolism - drug effects</subject><subject>Lipid Metabolism - genetics</subject><subject>Lipid Metabolism - physiology</subject><subject>Losartan - pharmacology</subject><subject>Lymphokines - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Norepinephrine - pharmacology</subject><subject>Pathology</subject><subject>platelet-derived growth factor</subject><subject>Platelet-Derived Growth Factor - metabolism</subject><subject>Proto-Oncogene Proteins c-sis - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, Platelet-Derived Growth Factor beta - metabolism</subject><subject>research-article</subject><subject>RNA, Messenger - metabolism</subject><subject>Vasoconstrictor Agents - pharmacology</subject><issn>0023-6837</issn><issn>1530-0307</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kU1P3DAQhi3UCra0P4ALiipxI3Qcf8QRp5avroQEh_YcOfYEDMFe7CyC_vp6m6h74zSW53lnrMeEHFA4ocDUt0F3zr9gGk9YDcCV3CELKhiUwKD-QBYAFSulYvUe-ZTSAwDlXIpdskdr4ExKviDDxesqYkou-EJ7WwzB6MH90ePmIvTF7fnVZfnjeKrnx_-YzbmIaHA1hlg4X4z3WDw66_FtE9H-zoURfcqd5bJ0vl8ntEXU42fysddDwi9z3Se_Ly9-nf0sr2-ulmffr0sjJIylaRrURlmpkCnBKXQN8KbhkvZIjap72yEyygxKKwzIzgghmkaAqRgzvWb75Os0dxXD8zr7aR_COvq8sq0qqJRsoM4QnSATQ0oR-3YV3ZOOby2FdqO3_a-3nfXmzOE8eN09od0mZp8ZOJoBnbLIPmpvXNpyijEOjGWumriUW_4O4_aF720_nUKY3b24HErGoTdoXf6NsbXBvZP-Cw2tqTg</recordid><startdate>20061201</startdate><enddate>20061201</enddate><creator>Ishizaka, Nobukazu</creator><creator>Matsuzaki, Gen</creator><creator>Saito, Kan</creator><creator>Noiri, Eisei</creator><creator>Mori, Ichiro</creator><creator>Nagai, Ryozo</creator><general>Elsevier Inc</general><general>Nature Publishing Group US</general><general>Nature Publishing</general><general>Nature Publishing Group</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20061201</creationdate><title>Expression and localization of PDGF-B, PDGF-D, and PDGF receptor in the kidney of angiotensin II-infused rat</title><author>Ishizaka, Nobukazu ; Matsuzaki, Gen ; Saito, Kan ; Noiri, Eisei ; Mori, Ichiro ; Nagai, Ryozo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c560t-c99eac8d68e385410b90499461fe1c87fdbee313ce6d5c06bc5559950c233cfa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>angiotensin II</topic><topic>Angiotensin II - pharmacology</topic><topic>Angiotensin II - physiology</topic><topic>Animals</topic><topic>Antihypertensive Agents - pharmacology</topic><topic>apoptosis</topic><topic>Apoptosis - physiology</topic><topic>Biological and medical sciences</topic><topic>Biotechnology</topic><topic>Cell Proliferation</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Hydralazine - pharmacology</topic><topic>hypertension</topic><topic>In Situ Hybridization</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Iron - metabolism</topic><topic>Kidney - metabolism</topic><topic>Kidney - physiology</topic><topic>Laboratory Medicine</topic><topic>lipid accumulation</topic><topic>Lipid Metabolism - drug effects</topic><topic>Lipid Metabolism - genetics</topic><topic>Lipid Metabolism - physiology</topic><topic>Losartan - pharmacology</topic><topic>Lymphokines - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Norepinephrine - pharmacology</topic><topic>Pathology</topic><topic>platelet-derived growth factor</topic><topic>Platelet-Derived Growth Factor - metabolism</topic><topic>Proto-Oncogene Proteins c-sis - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, Platelet-Derived Growth Factor beta - 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We have previously shown that long-term administration of angiotensin II in rats causes increased expression of transforming growth factor-β1, coupled with an accumulation of lipids in the tubular and vascular wall cells in the kidney. In this study, we examine the regulation of expression of platelet-derived growth factor (PDGF) and its receptor system and their co-localization with lipid deposits in the kidneys of angiotensin II-infused rats. Real-time RT-PCR showed that expression of PDGF-B, PDGF-D, and PDGF receptor-β (PDGFR-β) mRNA was increased by angiotensin II infusion, and in situ hybridization showed the co-localization of these mRNAs. Tubular cells that had increased PDGF-B mRNA expression were positive for lipid deposition and also for cellular proliferation, which was indicated by the presence of proliferating cell nuclear antigen. By contrast, in the kidneys of angiotensin II-infused rats, apoptosis occurred in tubular cells that contained deposits of iron but not lipids. The deposition of lipids and upregulation of PDGF-B, PDGF-D, and PDGFR-β induced by administration of angiotensin II were all suppressed by the selective angiotensin II type 1 (AT1) receptor antagonist losartan, but not by the nonspecific vasodilator hydralazine. The findings that lipid accumulation, upregulation of PDGF-B, PDGF-D, and PDGFR-β, and cellular proliferation were topologically associated and regulated in an AT1 receptor-dependent manner in the kidney of angiotensin II-infused rats suggests that these phenomena are related.</abstract><cop>New York</cop><pub>Elsevier Inc</pub><pmid>17043664</pmid><doi>10.1038/labinvest.3700486</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Laboratory investigation, 2006-12, Vol.86 (12), p.1285-1292 |
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| subjects | angiotensin II Angiotensin II - pharmacology Angiotensin II - physiology Animals Antihypertensive Agents - pharmacology apoptosis Apoptosis - physiology Biological and medical sciences Biotechnology Cell Proliferation Fundamental and applied biological sciences. Psychology Gene Expression Regulation - drug effects Hydralazine - pharmacology hypertension In Situ Hybridization Investigative techniques, diagnostic techniques (general aspects) Iron - metabolism Kidney - metabolism Kidney - physiology Laboratory Medicine lipid accumulation Lipid Metabolism - drug effects Lipid Metabolism - genetics Lipid Metabolism - physiology Losartan - pharmacology Lymphokines - metabolism Male Medical sciences Medicine Medicine & Public Health Norepinephrine - pharmacology Pathology platelet-derived growth factor Platelet-Derived Growth Factor - metabolism Proto-Oncogene Proteins c-sis - metabolism Rats Rats, Sprague-Dawley Receptor, Platelet-Derived Growth Factor beta - metabolism research-article RNA, Messenger - metabolism Vasoconstrictor Agents - pharmacology |
| title | Expression and localization of PDGF-B, PDGF-D, and PDGF receptor in the kidney of angiotensin II-infused rat |
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