Angiotensin II Removes Kidney Resistance Conferred by Ischemic Preconditioning
Ischemic preconditioning (IPC) by ischemia/reperfusion (I/R) renders resistance to the kidney. Strong IPC triggers kidney fibrosis, which is involved in angiotensin II (AngII) and its type 1 receptor (AT1R) signaling. Here, we investigated the role of AngII/AT1R signal pathway in the resistance of I...
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| description | Ischemic preconditioning (IPC) by ischemia/reperfusion (I/R) renders resistance to the kidney. Strong IPC triggers kidney fibrosis, which is involved in angiotensin II (AngII) and its type 1 receptor (AT1R) signaling. Here, we investigated the role of AngII/AT1R signal pathway in the resistance of IPC kidneys to subsequent I/R injury. IPC of kidneys was generated by 30 minutes of bilateral renal ischemia and 8 days of reperfusion. Sham-operation was performed to generate control (non-IPC) mice. To examine the roles of AngII and AT1R in IPC kidneys to subsequent I/R, IPC kidneys were subjected to either 30 minutes of bilateral kidney ischemia or sham-operation following treatment with AngII, losartan (AT1R blocker), or AngII plus losartan. IPC kidneys showed fibrotic changes, decreased AngII, and increased AT1R expression. I/R dramatically increased plasma creatinine concentrations in non-IPC mice, but not in IPC mice. AngII treatment in IPC mice resulted in enhanced morphological damage, oxidative stress, and inflammatory responses, with functional impairment, whereas losartan treatment reversed these effects. However, AngII treatment in non-IPC mice did not change I/R-induced injury. AngII abolished the resistance of IPC kidneys to subsequent I/R via the enhancement of oxidative stress and inflammatory responses, suggesting that the AngII/AT1R signaling pathway is associated with outcome in injury-experienced kidney. |
| doi_str_mv | 10.1155/2014/602149 |
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Strong IPC triggers kidney fibrosis, which is involved in angiotensin II (AngII) and its type 1 receptor (AT1R) signaling. Here, we investigated the role of AngII/AT1R signal pathway in the resistance of IPC kidneys to subsequent I/R injury. IPC of kidneys was generated by 30 minutes of bilateral renal ischemia and 8 days of reperfusion. Sham-operation was performed to generate control (non-IPC) mice. To examine the roles of AngII and AT1R in IPC kidneys to subsequent I/R, IPC kidneys were subjected to either 30 minutes of bilateral kidney ischemia or sham-operation following treatment with AngII, losartan (AT1R blocker), or AngII plus losartan. IPC kidneys showed fibrotic changes, decreased AngII, and increased AT1R expression. I/R dramatically increased plasma creatinine concentrations in non-IPC mice, but not in IPC mice. AngII treatment in IPC mice resulted in enhanced morphological damage, oxidative stress, and inflammatory responses, with functional impairment, whereas losartan treatment reversed these effects. However, AngII treatment in non-IPC mice did not change I/R-induced injury. AngII abolished the resistance of IPC kidneys to subsequent I/R via the enhancement of oxidative stress and inflammatory responses, suggesting that the AngII/AT1R signaling pathway is associated with outcome in injury-experienced kidney.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2014/602149</identifier><identifier>PMID: 25243156</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Angiotensin ; Angiotensin II - metabolism ; Animals ; Blood pressure ; Creatinine - blood ; Fibrosis ; Ischemia ; Ischemic Preconditioning - methods ; Kidney - pathology ; Kidney - physiopathology ; Kidney Diseases - metabolism ; Kidney Diseases - physiopathology ; Kidneys ; Lipid peroxidation ; Male ; Medicine ; Mice ; Mice, Inbred C57BL ; Oxidative Stress ; Physiological aspects ; Receptor, Angiotensin, Type 1 - metabolism ; Signal Transduction ; Studies</subject><ispartof>BioMed research international, 2014-01, Vol.2014 (2014), p.1-10</ispartof><rights>Copyright © 2014 Hee-Seong Jang et al.</rights><rights>COPYRIGHT 2014 John Wiley & Sons, Inc.</rights><rights>Copyright © 2014 Hee-Seong Jang et al. Hee-Seong Jang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2014 Hee-Seong Jang et al. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c594t-3eef7d642cf852062f32aaf3430c8afd1ba7d9bb1a0afea8635f5f1231c95dc03</citedby><cites>FETCH-LOGICAL-c594t-3eef7d642cf852062f32aaf3430c8afd1ba7d9bb1a0afea8635f5f1231c95dc03</cites><orcidid>0000-0002-1313-4791 ; 0000-0002-1617-5919 ; 0000-0002-9620-351X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4163347/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4163347/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27922,27923,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25243156$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Gildea, John J.</contributor><creatorcontrib>Park, Jeen-Woo</creatorcontrib><creatorcontrib>Kim, Jinu</creatorcontrib><creatorcontrib>Kim, Jee In</creatorcontrib><creatorcontrib>Jang, Hee-Seong</creatorcontrib><creatorcontrib>Park, Kwon Moo</creatorcontrib><title>Angiotensin II Removes Kidney Resistance Conferred by Ischemic Preconditioning</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Ischemic preconditioning (IPC) by ischemia/reperfusion (I/R) renders resistance to the kidney. Strong IPC triggers kidney fibrosis, which is involved in angiotensin II (AngII) and its type 1 receptor (AT1R) signaling. Here, we investigated the role of AngII/AT1R signal pathway in the resistance of IPC kidneys to subsequent I/R injury. IPC of kidneys was generated by 30 minutes of bilateral renal ischemia and 8 days of reperfusion. Sham-operation was performed to generate control (non-IPC) mice. To examine the roles of AngII and AT1R in IPC kidneys to subsequent I/R, IPC kidneys were subjected to either 30 minutes of bilateral kidney ischemia or sham-operation following treatment with AngII, losartan (AT1R blocker), or AngII plus losartan. IPC kidneys showed fibrotic changes, decreased AngII, and increased AT1R expression. I/R dramatically increased plasma creatinine concentrations in non-IPC mice, but not in IPC mice. AngII treatment in IPC mice resulted in enhanced morphological damage, oxidative stress, and inflammatory responses, with functional impairment, whereas losartan treatment reversed these effects. However, AngII treatment in non-IPC mice did not change I/R-induced injury. AngII abolished the resistance of IPC kidneys to subsequent I/R via the enhancement of oxidative stress and inflammatory responses, suggesting that the AngII/AT1R signaling pathway is associated with outcome in injury-experienced kidney.</description><subject>Angiotensin</subject><subject>Angiotensin II - metabolism</subject><subject>Animals</subject><subject>Blood pressure</subject><subject>Creatinine - blood</subject><subject>Fibrosis</subject><subject>Ischemia</subject><subject>Ischemic Preconditioning - methods</subject><subject>Kidney - pathology</subject><subject>Kidney - physiopathology</subject><subject>Kidney Diseases - metabolism</subject><subject>Kidney Diseases - physiopathology</subject><subject>Kidneys</subject><subject>Lipid peroxidation</subject><subject>Male</subject><subject>Medicine</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Oxidative Stress</subject><subject>Physiological aspects</subject><subject>Receptor, Angiotensin, Type 1 - metabolism</subject><subject>Signal Transduction</subject><subject>Studies</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><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>eNqN0c9rFDEUB_BBFFtqT95lwItUts3Lr8lchGXxx9KiInoOmczLbspMUpPZyv73Ztm61l5sLknIhy9571XVSyDnAEJcUAL8QhIKvH1SHVMGfCaBw9PDmbGj6jTna1KWAkla-bw6ooJyBkIeV5_nYeXjhCH7UC-X9Tcc4y3m-tL3Abflmn2eTLBYL2JwmBL2dbetl9mucfS2_prQxtD7ycfgw-pF9cyZIePp3X5S_fjw_vvi0-zqy8flYn41s6Ll04whuqaXnFqnBCWSOkaNcYwzYpVxPXSm6duuA0OMQ6MkE044KCXZVvSWsJPq3T73ZtON2FsMUzKDvkl-NGmro_H635fg13oVbzUHyRhvSsCbu4AUf24wT3r02eIwmIBxkzVIUCBYq_j_qZBSUUZpW-jrB_Q6blIondgpoqRShP5VKzOg9sHF8kW7C9VzTpsiGlBFvd0rm2LOCd2hOiB6N3u9m73ez77oV_cbcrB_Jl3A2R6sfejNL_-4NCwEnbmHS_-UYr8Be92-hQ</recordid><startdate>20140101</startdate><enddate>20140101</enddate><creator>Park, Jeen-Woo</creator><creator>Kim, Jinu</creator><creator>Kim, Jee In</creator><creator>Jang, Hee-Seong</creator><creator>Park, Kwon Moo</creator><general>Hindawi Publishing Corporation</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</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>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1313-4791</orcidid><orcidid>https://orcid.org/0000-0002-1617-5919</orcidid><orcidid>https://orcid.org/0000-0002-9620-351X</orcidid></search><sort><creationdate>20140101</creationdate><title>Angiotensin II Removes Kidney Resistance Conferred by Ischemic Preconditioning</title><author>Park, Jeen-Woo ; Kim, Jinu ; Kim, Jee In ; Jang, Hee-Seong ; Park, Kwon Moo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c594t-3eef7d642cf852062f32aaf3430c8afd1ba7d9bb1a0afea8635f5f1231c95dc03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Angiotensin</topic><topic>Angiotensin II - metabolism</topic><topic>Animals</topic><topic>Blood pressure</topic><topic>Creatinine - blood</topic><topic>Fibrosis</topic><topic>Ischemia</topic><topic>Ischemic Preconditioning - methods</topic><topic>Kidney - pathology</topic><topic>Kidney - physiopathology</topic><topic>Kidney Diseases - metabolism</topic><topic>Kidney Diseases - physiopathology</topic><topic>Kidneys</topic><topic>Lipid peroxidation</topic><topic>Male</topic><topic>Medicine</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Oxidative Stress</topic><topic>Physiological aspects</topic><topic>Receptor, Angiotensin, Type 1 - metabolism</topic><topic>Signal Transduction</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Park, Jeen-Woo</creatorcontrib><creatorcontrib>Kim, Jinu</creatorcontrib><creatorcontrib>Kim, Jee In</creatorcontrib><creatorcontrib>Jang, Hee-Seong</creatorcontrib><creatorcontrib>Park, Kwon Moo</creatorcontrib><collection>الدوريات العلمية والإحصائية - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Park, Jeen-Woo</au><au>Kim, Jinu</au><au>Kim, Jee In</au><au>Jang, Hee-Seong</au><au>Park, Kwon Moo</au><au>Gildea, John J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Angiotensin II Removes Kidney Resistance Conferred by Ischemic Preconditioning</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2014-01-01</date><risdate>2014</risdate><volume>2014</volume><issue>2014</issue><spage>1</spage><epage>10</epage><pages>1-10</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Ischemic preconditioning (IPC) by ischemia/reperfusion (I/R) renders resistance to the kidney. Strong IPC triggers kidney fibrosis, which is involved in angiotensin II (AngII) and its type 1 receptor (AT1R) signaling. Here, we investigated the role of AngII/AT1R signal pathway in the resistance of IPC kidneys to subsequent I/R injury. IPC of kidneys was generated by 30 minutes of bilateral renal ischemia and 8 days of reperfusion. Sham-operation was performed to generate control (non-IPC) mice. To examine the roles of AngII and AT1R in IPC kidneys to subsequent I/R, IPC kidneys were subjected to either 30 minutes of bilateral kidney ischemia or sham-operation following treatment with AngII, losartan (AT1R blocker), or AngII plus losartan. IPC kidneys showed fibrotic changes, decreased AngII, and increased AT1R expression. I/R dramatically increased plasma creatinine concentrations in non-IPC mice, but not in IPC mice. AngII treatment in IPC mice resulted in enhanced morphological damage, oxidative stress, and inflammatory responses, with functional impairment, whereas losartan treatment reversed these effects. However, AngII treatment in non-IPC mice did not change I/R-induced injury. AngII abolished the resistance of IPC kidneys to subsequent I/R via the enhancement of oxidative stress and inflammatory responses, suggesting that the AngII/AT1R signaling pathway is associated with outcome in injury-experienced kidney.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>25243156</pmid><doi>10.1155/2014/602149</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-1313-4791</orcidid><orcidid>https://orcid.org/0000-0002-1617-5919</orcidid><orcidid>https://orcid.org/0000-0002-9620-351X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Angiotensin Angiotensin II - metabolism Animals Blood pressure Creatinine - blood Fibrosis Ischemia Ischemic Preconditioning - methods Kidney - pathology Kidney - physiopathology Kidney Diseases - metabolism Kidney Diseases - physiopathology Kidneys Lipid peroxidation Male Medicine Mice Mice, Inbred C57BL Oxidative Stress Physiological aspects Receptor, Angiotensin, Type 1 - metabolism Signal Transduction Studies |
| title | Angiotensin II Removes Kidney Resistance Conferred by Ischemic Preconditioning |
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