15-Hydroxyprostaglandin dehydrogenase inhibitor prevents contrast-induced acute kidney injury
The two primary mechanisms by which iodinated contrast media (CM) causes contrast-induced acute kidney injury (CIAKI) are the hemodynamic effect causing intrarenal vasoconstriction and the tubular toxic effect causing acute tubular necrosis. Inhibition of 15-hydroxyprostaglandin dehydrogenase (15-PG...
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| description | The two primary mechanisms by which iodinated contrast media (CM) causes contrast-induced acute kidney injury (CIAKI) are the hemodynamic effect causing intrarenal vasoconstriction and the tubular toxic effect causing acute tubular necrosis. Inhibition of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), which degrades prostaglandin E
2
(PGE2), promotes tissue repair and regeneration in many organs. PGE2 causes intrarenal arterial vasodilation. In this study, we investigated whether a 15-PGDH inhibitor can act as a candidate for blocking these two major mechanisms of CIAKI. We established a CIAKI mouse model by injecting a 10 gram of iodine per body weight (gI/kg) dose of iodixanol into each mouse tail vein. A 15-PGDH inhibitor (SW033291), PGE1, or PGE2 were administered to compare the renal functional parameters, histologic injury, vasoconstriction, and renal blood flow changes. In addition, human renal proximal tubular epithelial cells were cultured in a CM-treated medium. SW033291, PGE1, or PGE2 were added to compare any changes in cell viability and apoptosis rate. CIAKI mice that received SW033291 had lower serum levels of creatinine, neutrophil gelatinase-associated lipocalin, and kidney injury molecule 1 (p |
| doi_str_mv | 10.1080/0886022X.2020.1870139 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmed_primary_33459127</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_e3eca66a95d348868256544b9625fae4</doaj_id><sourcerecordid>2721097429</sourcerecordid><originalsourceid>FETCH-LOGICAL-c562t-c257004b2786580dc6ed353f6f46001d9186cabaa4b936713ce0b5f36a51998e3</originalsourceid><addsrcrecordid>eNp9kstu1DAUhiMEokPhEUCR2LBJ8SW-bRCoKrRSJTYgsUGWY5_MeMjYg50U8vZ1mGlFWbCydPyf79z-qnqJ0RlGEr1FUnJEyLczgkgJSYEwVY-qFWaENRy16nG1WjTNIjqpnuW8RQgzKcjT6oTSlilMxKr6jllzObsUf8_7FPNo1oMJzofawWYJryGYDLUPG9_5MaZ6n-AGwphrG8OYTB4bH9xkwdXGTiPUP7wLMJeE7ZTm59WT3gwZXhzf0-rrx4sv55fN9edPV-cfrhvLOBkbS5hAqO2IkJxJ5CwHRxnted_y0rRTWHJrOmPaTlEuMLWAOtZTbhhWSgI9ra4OXBfNVu-T35k062i8_hOIaa1NGr0dQAMFazg3ijnalv1IwjhrC5gT1htoC-vdgbWfuh04C8uYwwPow5_gN3odb7SQlCgpCuDNEZDizwnyqHc-WxjKYiFOWZNWSCEkI0ut1_9It3FKoaxKE0EwUqIlqqjYQWXLhXKC_r4ZjPRiBn1nBr2YQR_NUPJe_T3Jfdbd9Yvg_UHgQx_TzvyKaXB6NPMQU59MsD5r-v8at8P4xRY</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2721097429</pqid></control><display><type>article</type><title>15-Hydroxyprostaglandin dehydrogenase inhibitor prevents contrast-induced acute kidney injury</title><source>Taylor & Francis Open Access</source><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Kim, Byeong Woo ; Kim, Hye Jung ; Kim, Sun-Hee ; Baik, Hyung Joo ; Kang, Mi Seon ; Kim, Dong-Hyun ; Markowitz, Sanford D. ; Kang, Sun Woo ; Bae, Ki Beom</creator><creatorcontrib>Kim, Byeong Woo ; Kim, Hye Jung ; Kim, Sun-Hee ; Baik, Hyung Joo ; Kang, Mi Seon ; Kim, Dong-Hyun ; Markowitz, Sanford D. ; Kang, Sun Woo ; Bae, Ki Beom</creatorcontrib><description><![CDATA[The two primary mechanisms by which iodinated contrast media (CM) causes contrast-induced acute kidney injury (CIAKI) are the hemodynamic effect causing intrarenal vasoconstriction and the tubular toxic effect causing acute tubular necrosis. Inhibition of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), which degrades prostaglandin E
2
(PGE2), promotes tissue repair and regeneration in many organs. PGE2 causes intrarenal arterial vasodilation. In this study, we investigated whether a 15-PGDH inhibitor can act as a candidate for blocking these two major mechanisms of CIAKI. We established a CIAKI mouse model by injecting a 10 gram of iodine per body weight (gI/kg) dose of iodixanol into each mouse tail vein. A 15-PGDH inhibitor (SW033291), PGE1, or PGE2 were administered to compare the renal functional parameters, histologic injury, vasoconstriction, and renal blood flow changes. In addition, human renal proximal tubular epithelial cells were cultured in a CM-treated medium. SW033291, PGE1, or PGE2 were added to compare any changes in cell viability and apoptosis rate. CIAKI mice that received SW033291 had lower serum levels of creatinine, neutrophil gelatinase-associated lipocalin, and kidney injury molecule 1 (p < 0.001); lower histologic injury score and TUNEL positive rates (p < 0.001); and higher medullary arteriolar area (p < 0.05) and renal blood flow (p < 0.001) than CM + vehicle group. In cell culture experiments, Adding SW033291 increased the viability rate (p < 0.05) and decreased the apoptosis rate of the tubular epithelial cells (p < 0.001). This 15-PGDH inhibitor blocks the two primary mechanisms of CIAKI, intrarenal vasoconstriction and tubular cell toxicity, and thus has the potential to be a novel prophylaxis for CIAKI. Abbreviations: 15-PGDH: 15-hydroxyprostaglandin dehydrogenase; AMP: adenosine monophosphate; CIAKI: contrast-induced acute kidney injury; CM: contrast media; EP: prostaglandin E2 receptor; hRPTECs: human-derived renal proximal tubule epithelial cells; KIM-1: kidney injury molecule-1; MTT: 3-(4,5-Dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide; NGAL: neutrophil gelatinase-associated lipocalin; PBS: phosphate-buffered saline; PGE1: prostaglandin E
1
; PGE2: prostaglandin E
2
; RBF: renal blood flow; TUNEL: terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling; α-SMA: α-Smooth muscle actin]]></description><identifier>ISSN: 0886-022X</identifier><identifier>ISSN: 1525-6049</identifier><identifier>EISSN: 1525-6049</identifier><identifier>DOI: 10.1080/0886022X.2020.1870139</identifier><identifier>PMID: 33459127</identifier><language>eng</language><publisher>England: Taylor & Francis</publisher><subject>15-Hydroxyprostaglandin dehydrogenase (NAD+) ; 15-PGDH inhibitor ; Actin ; Acute Kidney Injury - chemically induced ; Acute Kidney Injury - prevention & control ; AMP ; Animals ; Apoptosis ; Blood flow ; Body weight ; Cell culture ; Contrast agents ; Contrast media ; Contrast Media - adverse effects ; contrast media; acute kidney injury ; Creatinine ; Creatinine - blood ; Dehydrogenases ; DNA nucleotidylexotransferase ; Epithelial cells ; Female ; Gelatinase ; Humans ; Hydroxyprostaglandin Dehydrogenases - antagonists & inhibitors ; Iodine ; Kidney - physiopathology ; Kidneys ; Laboratory Study ; Leukocytes (neutrophilic) ; Lipocalin ; Lipocalin-2 - blood ; Mice ; Mice, Inbred C57BL ; Neutrophils ; Prophylaxis ; Prostaglandin E ; Prostaglandin E1 ; Prostaglandin E2 ; Prostaglandins E - pharmacology ; Pyridines - pharmacology ; Serum levels ; Smooth muscle ; Thiophenes - pharmacology ; Toxicity ; Triiodobenzoic Acids - adverse effects ; Vasoconstriction ; Vasodilation</subject><ispartof>Renal failure, 2021-01, Vol.43 (1), p.168-179</ispartof><rights>2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group 2021</rights><rights>2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This work is licensed under the Creative Commons Attribution – Non-Commercial License http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group 2021 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c562t-c257004b2786580dc6ed353f6f46001d9186cabaa4b936713ce0b5f36a51998e3</citedby><cites>FETCH-LOGICAL-c562t-c257004b2786580dc6ed353f6f46001d9186cabaa4b936713ce0b5f36a51998e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7832987/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7832987/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,27479,27901,27902,53766,53768,59116,59117</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33459127$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Byeong Woo</creatorcontrib><creatorcontrib>Kim, Hye Jung</creatorcontrib><creatorcontrib>Kim, Sun-Hee</creatorcontrib><creatorcontrib>Baik, Hyung Joo</creatorcontrib><creatorcontrib>Kang, Mi Seon</creatorcontrib><creatorcontrib>Kim, Dong-Hyun</creatorcontrib><creatorcontrib>Markowitz, Sanford D.</creatorcontrib><creatorcontrib>Kang, Sun Woo</creatorcontrib><creatorcontrib>Bae, Ki Beom</creatorcontrib><title>15-Hydroxyprostaglandin dehydrogenase inhibitor prevents contrast-induced acute kidney injury</title><title>Renal failure</title><addtitle>Ren Fail</addtitle><description><![CDATA[The two primary mechanisms by which iodinated contrast media (CM) causes contrast-induced acute kidney injury (CIAKI) are the hemodynamic effect causing intrarenal vasoconstriction and the tubular toxic effect causing acute tubular necrosis. Inhibition of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), which degrades prostaglandin E
2
(PGE2), promotes tissue repair and regeneration in many organs. PGE2 causes intrarenal arterial vasodilation. In this study, we investigated whether a 15-PGDH inhibitor can act as a candidate for blocking these two major mechanisms of CIAKI. We established a CIAKI mouse model by injecting a 10 gram of iodine per body weight (gI/kg) dose of iodixanol into each mouse tail vein. A 15-PGDH inhibitor (SW033291), PGE1, or PGE2 were administered to compare the renal functional parameters, histologic injury, vasoconstriction, and renal blood flow changes. In addition, human renal proximal tubular epithelial cells were cultured in a CM-treated medium. SW033291, PGE1, or PGE2 were added to compare any changes in cell viability and apoptosis rate. CIAKI mice that received SW033291 had lower serum levels of creatinine, neutrophil gelatinase-associated lipocalin, and kidney injury molecule 1 (p < 0.001); lower histologic injury score and TUNEL positive rates (p < 0.001); and higher medullary arteriolar area (p < 0.05) and renal blood flow (p < 0.001) than CM + vehicle group. In cell culture experiments, Adding SW033291 increased the viability rate (p < 0.05) and decreased the apoptosis rate of the tubular epithelial cells (p < 0.001). This 15-PGDH inhibitor blocks the two primary mechanisms of CIAKI, intrarenal vasoconstriction and tubular cell toxicity, and thus has the potential to be a novel prophylaxis for CIAKI. Abbreviations: 15-PGDH: 15-hydroxyprostaglandin dehydrogenase; AMP: adenosine monophosphate; CIAKI: contrast-induced acute kidney injury; CM: contrast media; EP: prostaglandin E2 receptor; hRPTECs: human-derived renal proximal tubule epithelial cells; KIM-1: kidney injury molecule-1; MTT: 3-(4,5-Dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide; NGAL: neutrophil gelatinase-associated lipocalin; PBS: phosphate-buffered saline; PGE1: prostaglandin E
1
; PGE2: prostaglandin E
2
; RBF: renal blood flow; TUNEL: terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling; α-SMA: α-Smooth muscle actin]]></description><subject>15-Hydroxyprostaglandin dehydrogenase (NAD+)</subject><subject>15-PGDH inhibitor</subject><subject>Actin</subject><subject>Acute Kidney Injury - chemically induced</subject><subject>Acute Kidney Injury - prevention & control</subject><subject>AMP</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Blood flow</subject><subject>Body weight</subject><subject>Cell culture</subject><subject>Contrast agents</subject><subject>Contrast media</subject><subject>Contrast Media - adverse effects</subject><subject>contrast media; acute kidney injury</subject><subject>Creatinine</subject><subject>Creatinine - blood</subject><subject>Dehydrogenases</subject><subject>DNA nucleotidylexotransferase</subject><subject>Epithelial cells</subject><subject>Female</subject><subject>Gelatinase</subject><subject>Humans</subject><subject>Hydroxyprostaglandin Dehydrogenases - antagonists & inhibitors</subject><subject>Iodine</subject><subject>Kidney - physiopathology</subject><subject>Kidneys</subject><subject>Laboratory Study</subject><subject>Leukocytes (neutrophilic)</subject><subject>Lipocalin</subject><subject>Lipocalin-2 - blood</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Neutrophils</subject><subject>Prophylaxis</subject><subject>Prostaglandin E</subject><subject>Prostaglandin E1</subject><subject>Prostaglandin E2</subject><subject>Prostaglandins E - pharmacology</subject><subject>Pyridines - pharmacology</subject><subject>Serum levels</subject><subject>Smooth muscle</subject><subject>Thiophenes - pharmacology</subject><subject>Toxicity</subject><subject>Triiodobenzoic Acids - adverse effects</subject><subject>Vasoconstriction</subject><subject>Vasodilation</subject><issn>0886-022X</issn><issn>1525-6049</issn><issn>1525-6049</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><sourceid>DOA</sourceid><recordid>eNp9kstu1DAUhiMEokPhEUCR2LBJ8SW-bRCoKrRSJTYgsUGWY5_MeMjYg50U8vZ1mGlFWbCydPyf79z-qnqJ0RlGEr1FUnJEyLczgkgJSYEwVY-qFWaENRy16nG1WjTNIjqpnuW8RQgzKcjT6oTSlilMxKr6jllzObsUf8_7FPNo1oMJzofawWYJryGYDLUPG9_5MaZ6n-AGwphrG8OYTB4bH9xkwdXGTiPUP7wLMJeE7ZTm59WT3gwZXhzf0-rrx4sv55fN9edPV-cfrhvLOBkbS5hAqO2IkJxJ5CwHRxnted_y0rRTWHJrOmPaTlEuMLWAOtZTbhhWSgI9ra4OXBfNVu-T35k062i8_hOIaa1NGr0dQAMFazg3ijnalv1IwjhrC5gT1htoC-vdgbWfuh04C8uYwwPow5_gN3odb7SQlCgpCuDNEZDizwnyqHc-WxjKYiFOWZNWSCEkI0ut1_9It3FKoaxKE0EwUqIlqqjYQWXLhXKC_r4ZjPRiBn1nBr2YQR_NUPJe_T3Jfdbd9Yvg_UHgQx_TzvyKaXB6NPMQU59MsD5r-v8at8P4xRY</recordid><startdate>20210101</startdate><enddate>20210101</enddate><creator>Kim, Byeong Woo</creator><creator>Kim, Hye Jung</creator><creator>Kim, Sun-Hee</creator><creator>Baik, Hyung Joo</creator><creator>Kang, Mi Seon</creator><creator>Kim, Dong-Hyun</creator><creator>Markowitz, Sanford D.</creator><creator>Kang, Sun Woo</creator><creator>Bae, Ki Beom</creator><general>Taylor & Francis</general><general>Taylor & Francis Ltd</general><general>Taylor & Francis Group</general><scope>0YH</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>7T5</scope><scope>7XB</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20210101</creationdate><title>15-Hydroxyprostaglandin dehydrogenase inhibitor prevents contrast-induced acute kidney injury</title><author>Kim, Byeong Woo ; Kim, Hye Jung ; Kim, Sun-Hee ; Baik, Hyung Joo ; Kang, Mi Seon ; Kim, Dong-Hyun ; Markowitz, Sanford D. ; Kang, Sun Woo ; Bae, Ki Beom</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c562t-c257004b2786580dc6ed353f6f46001d9186cabaa4b936713ce0b5f36a51998e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>15-Hydroxyprostaglandin dehydrogenase (NAD+)</topic><topic>15-PGDH inhibitor</topic><topic>Actin</topic><topic>Acute Kidney Injury - chemically induced</topic><topic>Acute Kidney Injury - prevention & control</topic><topic>AMP</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Blood flow</topic><topic>Body weight</topic><topic>Cell culture</topic><topic>Contrast agents</topic><topic>Contrast media</topic><topic>Contrast Media - adverse effects</topic><topic>contrast media; acute kidney injury</topic><topic>Creatinine</topic><topic>Creatinine - blood</topic><topic>Dehydrogenases</topic><topic>DNA nucleotidylexotransferase</topic><topic>Epithelial cells</topic><topic>Female</topic><topic>Gelatinase</topic><topic>Humans</topic><topic>Hydroxyprostaglandin Dehydrogenases - antagonists & inhibitors</topic><topic>Iodine</topic><topic>Kidney - physiopathology</topic><topic>Kidneys</topic><topic>Laboratory Study</topic><topic>Leukocytes (neutrophilic)</topic><topic>Lipocalin</topic><topic>Lipocalin-2 - blood</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Neutrophils</topic><topic>Prophylaxis</topic><topic>Prostaglandin E</topic><topic>Prostaglandin E1</topic><topic>Prostaglandin E2</topic><topic>Prostaglandins E - pharmacology</topic><topic>Pyridines - pharmacology</topic><topic>Serum levels</topic><topic>Smooth muscle</topic><topic>Thiophenes - pharmacology</topic><topic>Toxicity</topic><topic>Triiodobenzoic Acids - adverse effects</topic><topic>Vasoconstriction</topic><topic>Vasodilation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Byeong Woo</creatorcontrib><creatorcontrib>Kim, Hye Jung</creatorcontrib><creatorcontrib>Kim, Sun-Hee</creatorcontrib><creatorcontrib>Baik, Hyung Joo</creatorcontrib><creatorcontrib>Kang, Mi Seon</creatorcontrib><creatorcontrib>Kim, Dong-Hyun</creatorcontrib><creatorcontrib>Markowitz, Sanford D.</creatorcontrib><creatorcontrib>Kang, Sun Woo</creatorcontrib><creatorcontrib>Bae, Ki Beom</creatorcontrib><collection>Taylor & Francis Open Access</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>Immunology Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Renal failure</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Byeong Woo</au><au>Kim, Hye Jung</au><au>Kim, Sun-Hee</au><au>Baik, Hyung Joo</au><au>Kang, Mi Seon</au><au>Kim, Dong-Hyun</au><au>Markowitz, Sanford D.</au><au>Kang, Sun Woo</au><au>Bae, Ki Beom</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>15-Hydroxyprostaglandin dehydrogenase inhibitor prevents contrast-induced acute kidney injury</atitle><jtitle>Renal failure</jtitle><addtitle>Ren Fail</addtitle><date>2021-01-01</date><risdate>2021</risdate><volume>43</volume><issue>1</issue><spage>168</spage><epage>179</epage><pages>168-179</pages><issn>0886-022X</issn><issn>1525-6049</issn><eissn>1525-6049</eissn><abstract><![CDATA[The two primary mechanisms by which iodinated contrast media (CM) causes contrast-induced acute kidney injury (CIAKI) are the hemodynamic effect causing intrarenal vasoconstriction and the tubular toxic effect causing acute tubular necrosis. Inhibition of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), which degrades prostaglandin E
2
(PGE2), promotes tissue repair and regeneration in many organs. PGE2 causes intrarenal arterial vasodilation. In this study, we investigated whether a 15-PGDH inhibitor can act as a candidate for blocking these two major mechanisms of CIAKI. We established a CIAKI mouse model by injecting a 10 gram of iodine per body weight (gI/kg) dose of iodixanol into each mouse tail vein. A 15-PGDH inhibitor (SW033291), PGE1, or PGE2 were administered to compare the renal functional parameters, histologic injury, vasoconstriction, and renal blood flow changes. In addition, human renal proximal tubular epithelial cells were cultured in a CM-treated medium. SW033291, PGE1, or PGE2 were added to compare any changes in cell viability and apoptosis rate. CIAKI mice that received SW033291 had lower serum levels of creatinine, neutrophil gelatinase-associated lipocalin, and kidney injury molecule 1 (p < 0.001); lower histologic injury score and TUNEL positive rates (p < 0.001); and higher medullary arteriolar area (p < 0.05) and renal blood flow (p < 0.001) than CM + vehicle group. In cell culture experiments, Adding SW033291 increased the viability rate (p < 0.05) and decreased the apoptosis rate of the tubular epithelial cells (p < 0.001). This 15-PGDH inhibitor blocks the two primary mechanisms of CIAKI, intrarenal vasoconstriction and tubular cell toxicity, and thus has the potential to be a novel prophylaxis for CIAKI. Abbreviations: 15-PGDH: 15-hydroxyprostaglandin dehydrogenase; AMP: adenosine monophosphate; CIAKI: contrast-induced acute kidney injury; CM: contrast media; EP: prostaglandin E2 receptor; hRPTECs: human-derived renal proximal tubule epithelial cells; KIM-1: kidney injury molecule-1; MTT: 3-(4,5-Dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide; NGAL: neutrophil gelatinase-associated lipocalin; PBS: phosphate-buffered saline; PGE1: prostaglandin E
1
; PGE2: prostaglandin E
2
; RBF: renal blood flow; TUNEL: terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling; α-SMA: α-Smooth muscle actin]]></abstract><cop>England</cop><pub>Taylor & Francis</pub><pmid>33459127</pmid><doi>10.1080/0886022X.2020.1870139</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Renal failure, 2021-01, Vol.43 (1), p.168-179 |
| issn | 0886-022X 1525-6049 1525-6049 |
| language | eng |
| recordid | cdi_pubmed_primary_33459127 |
| source | Taylor & Francis Open Access; MEDLINE; DOAJ Directory of Open Access Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | 15-Hydroxyprostaglandin dehydrogenase (NAD+) 15-PGDH inhibitor Actin Acute Kidney Injury - chemically induced Acute Kidney Injury - prevention & control AMP Animals Apoptosis Blood flow Body weight Cell culture Contrast agents Contrast media Contrast Media - adverse effects contrast media acute kidney injury Creatinine Creatinine - blood Dehydrogenases DNA nucleotidylexotransferase Epithelial cells Female Gelatinase Humans Hydroxyprostaglandin Dehydrogenases - antagonists & inhibitors Iodine Kidney - physiopathology Kidneys Laboratory Study Leukocytes (neutrophilic) Lipocalin Lipocalin-2 - blood Mice Mice, Inbred C57BL Neutrophils Prophylaxis Prostaglandin E Prostaglandin E1 Prostaglandin E2 Prostaglandins E - pharmacology Pyridines - pharmacology Serum levels Smooth muscle Thiophenes - pharmacology Toxicity Triiodobenzoic Acids - adverse effects Vasoconstriction Vasodilation |
| title | 15-Hydroxyprostaglandin dehydrogenase inhibitor prevents contrast-induced acute kidney injury |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-07T11%3A01%3A46IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=15-Hydroxyprostaglandin%20dehydrogenase%20inhibitor%20prevents%20contrast-induced%20acute%20kidney%20injury&rft.jtitle=Renal%20failure&rft.au=Kim,%20Byeong%20Woo&rft.date=2021-01-01&rft.volume=43&rft.issue=1&rft.spage=168&rft.epage=179&rft.pages=168-179&rft.issn=0886-022X&rft.eissn=1525-6049&rft_id=info:doi/10.1080/0886022X.2020.1870139&rft_dat=%3Cproquest_pubme%3E2721097429%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2721097429&rft_id=info:pmid/33459127&rft_doaj_id=oai_doaj_org_article_e3eca66a95d348868256544b9625fae4&rfr_iscdi=true |