Paricalcitol Attenuates Contrast-Induced Acute Kidney Injury by Regulating Mitophagy and Senescence
Contrast-induced acute kidney injury (CI-AKI) is the third most common cause of hospital-acquired renal failure, with an incidence of 11%. However, the disease mechanism remains unclear, and no effective treatment is available. Paricalcitol has been reported to be effective in animal models of kidne...
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description | Contrast-induced acute kidney injury (CI-AKI) is the third most common cause of hospital-acquired renal failure, with an incidence of 11%. However, the disease mechanism remains unclear, and no effective treatment is available. Paricalcitol has been reported to be effective in animal models of kidney injury. We hypothesized that paricalcitol could play a renoprotective role against CI-AKI. Rats were divided into control, paricalcitol, contrast, and paricalcitol-plus-contrast groups. We used a previously published protocol to produce CI-AKI. Paricalcitol (0.3 μg/kg) was administered intraperitoneally before 24 h and 30 min before indomethacin. We used HK-2 cells to evaluate the effects of paricalcitol on mitophagy and senescence. Ioversol triggered renal dysfunction, increasing blood urea nitrogen and serum creatinine. Significant tubular damage, increased 8-OHdG expression, and apoptosis were apparent. Ioversol injection induced high expression levels of the mitophagy markers Pink1, Parkin, and LC3 and the senescence markers β-galactosidase and p16INK4A. Paricalcitol pretreatment prevented renal dysfunction and reduced tissue damage by reducing both mitophagy and senescence. Cellular morphological changes were found, and expression of LC3B and HMGB1 was increased by ioversol in HK-2 cells. Paricalcitol countered these effects. This study showed that mitochondria might drive injury phenotypes in CI-AKI, and that paricalcitol protects against CI-AKI by decreasing mitochondrial damage. |
doi_str_mv | 10.1155/2020/7627934 |
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However, the disease mechanism remains unclear, and no effective treatment is available. Paricalcitol has been reported to be effective in animal models of kidney injury. We hypothesized that paricalcitol could play a renoprotective role against CI-AKI. Rats were divided into control, paricalcitol, contrast, and paricalcitol-plus-contrast groups. We used a previously published protocol to produce CI-AKI. Paricalcitol (0.3 μg/kg) was administered intraperitoneally before 24 h and 30 min before indomethacin. We used HK-2 cells to evaluate the effects of paricalcitol on mitophagy and senescence. Ioversol triggered renal dysfunction, increasing blood urea nitrogen and serum creatinine. Significant tubular damage, increased 8-OHdG expression, and apoptosis were apparent. Ioversol injection induced high expression levels of the mitophagy markers Pink1, Parkin, and LC3 and the senescence markers β-galactosidase and p16INK4A. Paricalcitol pretreatment prevented renal dysfunction and reduced tissue damage by reducing both mitophagy and senescence. Cellular morphological changes were found, and expression of LC3B and HMGB1 was increased by ioversol in HK-2 cells. Paricalcitol countered these effects. This study showed that mitochondria might drive injury phenotypes in CI-AKI, and that paricalcitol protects against CI-AKI by decreasing mitochondrial damage.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2020/7627934</identifier><identifier>PMID: 33299530</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Antibodies ; Apoptosis ; Autophagy ; Cell cycle ; Ischemia ; Kidneys ; Laboratory animals ; Mitochondria ; Oxidative stress ; Pathology ; Senescence</subject><ispartof>Oxidative medicine and cellular longevity, 2020, Vol.2020 (2020), p.1-13</ispartof><rights>Copyright © 2020 Eunjin Bae et al.</rights><rights>Copyright © 2020 Eunjin Bae et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2020 Eunjin Bae et al. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-6a1efb0dcabf51f3527dbb9fadc1190769ec9edaeac2818b96e6fbd7a006be953</citedby><cites>FETCH-LOGICAL-c448t-6a1efb0dcabf51f3527dbb9fadc1190769ec9edaeac2818b96e6fbd7a006be953</cites><orcidid>0000-0001-5233-537X</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/PMC7704155/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7704155/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4024,27923,27924,27925,53791,53793</link.rule.ids></links><search><contributor>Braun, Ralf</contributor><contributor>Ralf Braun</contributor><creatorcontrib>Park, Dong Jun</creatorcontrib><creatorcontrib>Chang, Se-Ho</creatorcontrib><creatorcontrib>Lee, Seunghye</creatorcontrib><creatorcontrib>Jung, Sehyun</creatorcontrib><creatorcontrib>Lee, Tae Won</creatorcontrib><creatorcontrib>Jang, Si Jung</creatorcontrib><creatorcontrib>Jung, Myeong Hee</creatorcontrib><creatorcontrib>Kim, Jin Hyun</creatorcontrib><creatorcontrib>Bae, Eunjin</creatorcontrib><creatorcontrib>Jang, Ha Nee</creatorcontrib><title>Paricalcitol Attenuates Contrast-Induced Acute Kidney Injury by Regulating Mitophagy and Senescence</title><title>Oxidative medicine and cellular longevity</title><description>Contrast-induced acute kidney injury (CI-AKI) is the third most common cause of hospital-acquired renal failure, with an incidence of 11%. However, the disease mechanism remains unclear, and no effective treatment is available. Paricalcitol has been reported to be effective in animal models of kidney injury. We hypothesized that paricalcitol could play a renoprotective role against CI-AKI. Rats were divided into control, paricalcitol, contrast, and paricalcitol-plus-contrast groups. We used a previously published protocol to produce CI-AKI. Paricalcitol (0.3 μg/kg) was administered intraperitoneally before 24 h and 30 min before indomethacin. We used HK-2 cells to evaluate the effects of paricalcitol on mitophagy and senescence. Ioversol triggered renal dysfunction, increasing blood urea nitrogen and serum creatinine. Significant tubular damage, increased 8-OHdG expression, and apoptosis were apparent. Ioversol injection induced high expression levels of the mitophagy markers Pink1, Parkin, and LC3 and the senescence markers β-galactosidase and p16INK4A. Paricalcitol pretreatment prevented renal dysfunction and reduced tissue damage by reducing both mitophagy and senescence. Cellular morphological changes were found, and expression of LC3B and HMGB1 was increased by ioversol in HK-2 cells. Paricalcitol countered these effects. This study showed that mitochondria might drive injury phenotypes in CI-AKI, and that paricalcitol protects against CI-AKI by decreasing mitochondrial damage.</description><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Cell cycle</subject><subject>Ischemia</subject><subject>Kidneys</subject><subject>Laboratory animals</subject><subject>Mitochondria</subject><subject>Oxidative stress</subject><subject>Pathology</subject><subject>Senescence</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkc-L1DAYhou4uOvqzbMEvAhr3SRNm8lFGIZVh11R_HEOX5KvMxk66WyTKv3vTZlhRS-eEsjDm-_53qJ4wehbxur6mlNOr2XDparEo-KCKcFLqpR4_HCn9Lx4GuOO0qbigj0pzquKK1VX9KKwX2DwFjrrU9-RZUoYRkgYyaoPaYCYynVwo0VHlnZMSG69CziRddiNw0TMRL7iZuwg-bAhn3LGYQubiUBw5BsGjBaDxWfFWQtdxOen87L48f7m--pjeff5w3q1vCutEItUNsCwNdRZMG3N2qrm0hmjWnCWMUVlo9AqdIBg-YItjGqwaY2TkL0MZp3L4t0x9zCaPbr8dzbo9GHwexgm3YPXf78Ev9Wb_qeWkoq8yhzw-hQw9PcjxqT3Pit0HQTsx6i5aPIcrKYz-uofdNePQ8h6MyVr2ig5U2-OlB36GAdsH4ZhVM_t6bk9fWov41dHfOuDg1_-f_TLI42ZwRb-0JzWgsrqN6JPpI4</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>Park, Dong Jun</creator><creator>Chang, Se-Ho</creator><creator>Lee, Seunghye</creator><creator>Jung, Sehyun</creator><creator>Lee, Tae Won</creator><creator>Jang, Si Jung</creator><creator>Jung, Myeong Hee</creator><creator>Kim, Jin Hyun</creator><creator>Bae, Eunjin</creator><creator>Jang, Ha Nee</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</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>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</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><orcidid>https://orcid.org/0000-0001-5233-537X</orcidid></search><sort><creationdate>2020</creationdate><title>Paricalcitol Attenuates Contrast-Induced Acute Kidney Injury by Regulating Mitophagy and Senescence</title><author>Park, Dong Jun ; 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However, the disease mechanism remains unclear, and no effective treatment is available. Paricalcitol has been reported to be effective in animal models of kidney injury. We hypothesized that paricalcitol could play a renoprotective role against CI-AKI. Rats were divided into control, paricalcitol, contrast, and paricalcitol-plus-contrast groups. We used a previously published protocol to produce CI-AKI. Paricalcitol (0.3 μg/kg) was administered intraperitoneally before 24 h and 30 min before indomethacin. We used HK-2 cells to evaluate the effects of paricalcitol on mitophagy and senescence. Ioversol triggered renal dysfunction, increasing blood urea nitrogen and serum creatinine. Significant tubular damage, increased 8-OHdG expression, and apoptosis were apparent. Ioversol injection induced high expression levels of the mitophagy markers Pink1, Parkin, and LC3 and the senescence markers β-galactosidase and p16INK4A. Paricalcitol pretreatment prevented renal dysfunction and reduced tissue damage by reducing both mitophagy and senescence. Cellular morphological changes were found, and expression of LC3B and HMGB1 was increased by ioversol in HK-2 cells. Paricalcitol countered these effects. This study showed that mitochondria might drive injury phenotypes in CI-AKI, and that paricalcitol protects against CI-AKI by decreasing mitochondrial damage.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>33299530</pmid><doi>10.1155/2020/7627934</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-5233-537X</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Antibodies Apoptosis Autophagy Cell cycle Ischemia Kidneys Laboratory animals Mitochondria Oxidative stress Pathology Senescence |
title | Paricalcitol Attenuates Contrast-Induced Acute Kidney Injury by Regulating Mitophagy and Senescence |
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