SerpinA3K Deficiency Reduces Oxidative Stress in Acute Kidney Injury
We previously showed that SerpinA3K is present in urine from rats and humans with acute kidney injury (AKI) and chronic kidney disease (CKD). However, the specific role of SerpinA3K during renal pathophysiology is unknown. To begin to understand the role of SerpinA3K on AKI, SerpinA3K-deficient (KOS...
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| Veröffentlicht in: | International journal of molecular sciences 2023-04, Vol.24 (9), p.7815 |
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| creator | González-Soria, Isaac Soto-Valadez, Axel D Martínez-Rojas, Miguel Angel Ortega-Trejo, Juan Antonio Pérez-Villalva, Rosalba Gamba, Gerardo Sánchez-Navarro, Andrea Bobadilla, Norma A |
| description | We previously showed that SerpinA3K is present in urine from rats and humans with acute kidney injury (AKI) and chronic kidney disease (CKD). However, the specific role of SerpinA3K during renal pathophysiology is unknown. To begin to understand the role of SerpinA3K on AKI, SerpinA3K-deficient (KOSA3) mice were studied 24 h after inducing ischemia/reperfusion (I/R) and compared to wild type (WT) mice. Four groups were studied: WT+S, WT+IR, KOSA3+S, and KOSA3+IR. As expected, I/R increased serum creatinine and BUN, with a GFR reduction in both genotypes; however, renal dysfunction was ameliorated in the KOSA3+IR group. Interestingly, the increase in UH
O
induced by I/R was not equally seen in the KOSA3+IR group, an effect that was associated with the preservation of antioxidant enzymes' mRNA levels. Additionally, FOXO3 expression was initially greater in the KOSA3 than in the WT group. Moreover, the increase in BAX protein level and the decrease in
and
induced by I/R were not observed in the KOSA3+IR group, suggesting that these animals have better cellular responses to hypoxic injury. Our findings suggest that SerpinA3K is involved in the renal oxidant response, HIF1α/VEGF pathway, and cell apoptosis. |
| doi_str_mv | 10.3390/ijms24097815 |
| format | Article |
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O
induced by I/R was not equally seen in the KOSA3+IR group, an effect that was associated with the preservation of antioxidant enzymes' mRNA levels. Additionally, FOXO3 expression was initially greater in the KOSA3 than in the WT group. Moreover, the increase in BAX protein level and the decrease in
and
induced by I/R were not observed in the KOSA3+IR group, suggesting that these animals have better cellular responses to hypoxic injury. Our findings suggest that SerpinA3K is involved in the renal oxidant response, HIF1α/VEGF pathway, and cell apoptosis.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms24097815</identifier><identifier>PMID: 37175519</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Acute Kidney Injury - metabolism ; Animals ; Apoptosis ; BAX protein ; Biomarkers ; Creatinine ; Cytokines ; FOXO3 protein ; Gene expression ; Genotypes ; Hypoxia ; Injury prevention ; Ischemia ; Kidney - metabolism ; Kidney diseases ; Kidneys ; Mice ; Morphology ; Mortality ; mRNA ; Oxidants ; Oxidative Stress ; Oxidizing agents ; Proteins ; Renal function ; Renal Insufficiency, Chronic - metabolism ; Reperfusion ; Reperfusion Injury - metabolism ; Severe acute respiratory syndrome coronavirus 2 ; Vascular endothelial growth factor</subject><ispartof>International journal of molecular sciences, 2023-04, Vol.24 (9), p.7815</ispartof><rights>COPYRIGHT 2023 MDPI AG</rights><rights>2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2023 by the authors. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c480t-1a2968268b34a4a106b868667045090d57316dafd8e2d3c7016ee88a3b8a75c93</citedby><cites>FETCH-LOGICAL-c480t-1a2968268b34a4a106b868667045090d57316dafd8e2d3c7016ee88a3b8a75c93</cites><orcidid>0000-0002-4378-9043 ; 0000-0003-2344-0319 ; 0000-0002-9171-4206 ; 0000-0003-1060-5567 ; 0000-0001-5671-7770</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/PMC10177890/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10177890/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37175519$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>González-Soria, Isaac</creatorcontrib><creatorcontrib>Soto-Valadez, Axel D</creatorcontrib><creatorcontrib>Martínez-Rojas, Miguel Angel</creatorcontrib><creatorcontrib>Ortega-Trejo, Juan Antonio</creatorcontrib><creatorcontrib>Pérez-Villalva, Rosalba</creatorcontrib><creatorcontrib>Gamba, Gerardo</creatorcontrib><creatorcontrib>Sánchez-Navarro, Andrea</creatorcontrib><creatorcontrib>Bobadilla, Norma A</creatorcontrib><title>SerpinA3K Deficiency Reduces Oxidative Stress in Acute Kidney Injury</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>We previously showed that SerpinA3K is present in urine from rats and humans with acute kidney injury (AKI) and chronic kidney disease (CKD). However, the specific role of SerpinA3K during renal pathophysiology is unknown. To begin to understand the role of SerpinA3K on AKI, SerpinA3K-deficient (KOSA3) mice were studied 24 h after inducing ischemia/reperfusion (I/R) and compared to wild type (WT) mice. Four groups were studied: WT+S, WT+IR, KOSA3+S, and KOSA3+IR. As expected, I/R increased serum creatinine and BUN, with a GFR reduction in both genotypes; however, renal dysfunction was ameliorated in the KOSA3+IR group. Interestingly, the increase in UH
O
induced by I/R was not equally seen in the KOSA3+IR group, an effect that was associated with the preservation of antioxidant enzymes' mRNA levels. Additionally, FOXO3 expression was initially greater in the KOSA3 than in the WT group. Moreover, the increase in BAX protein level and the decrease in
and
induced by I/R were not observed in the KOSA3+IR group, suggesting that these animals have better cellular responses to hypoxic injury. Our findings suggest that SerpinA3K is involved in the renal oxidant response, HIF1α/VEGF pathway, and cell apoptosis.</description><subject>Acute Kidney Injury - metabolism</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>BAX protein</subject><subject>Biomarkers</subject><subject>Creatinine</subject><subject>Cytokines</subject><subject>FOXO3 protein</subject><subject>Gene expression</subject><subject>Genotypes</subject><subject>Hypoxia</subject><subject>Injury prevention</subject><subject>Ischemia</subject><subject>Kidney - metabolism</subject><subject>Kidney diseases</subject><subject>Kidneys</subject><subject>Mice</subject><subject>Morphology</subject><subject>Mortality</subject><subject>mRNA</subject><subject>Oxidants</subject><subject>Oxidative Stress</subject><subject>Oxidizing agents</subject><subject>Proteins</subject><subject>Renal function</subject><subject>Renal Insufficiency, Chronic - metabolism</subject><subject>Reperfusion</subject><subject>Reperfusion Injury - metabolism</subject><subject>Severe acute respiratory syndrome coronavirus 2</subject><subject>Vascular endothelial growth factor</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</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>eNptkctPHDEMxiNUVCjtjXM1Ui8cupD341StoA8EElJpz1E28dCsZjLbZAax_z1ZQemCkA-2kp8_y_4QOiT4mDGDT-KyL5RjozQRO2ifcEpnGEv1ZqveQ-9KWWJMGRXmLdpjiighiNlHZ9eQVzHN2UVzBm30EZJfNz8hTB5Kc3UXgxvjLTTXY4ZSmpiauZ9GaC5iSLBuztNyyuv3aLd1XYEPj_kA_f729dfpj9nl1ffz0_nlzHONxxlx1EhNpV4w7rgjWC601FIqzAU2OAjFiAyuDRpoYF5hIgG0dmyhnRLesAP05UF3NS16CB7SmF1nVzn2Lq_t4KJ9_pPiH3sz3FqCiVLa4Kpw9KiQh78TlNH2sXjoOpdgmIqlmjAhuaG8op9eoMthyqnut6GoEJhT85-6cR3YmNqhDvYbUTtXgvJNsEodv0LVCNBHP6R6-fr-rOHzQ4PPQykZ2qclCbYb2-227RX_uH2YJ_ifz-weCDylWg</recordid><startdate>20230425</startdate><enddate>20230425</enddate><creator>González-Soria, Isaac</creator><creator>Soto-Valadez, Axel D</creator><creator>Martínez-Rojas, Miguel Angel</creator><creator>Ortega-Trejo, Juan Antonio</creator><creator>Pérez-Villalva, Rosalba</creator><creator>Gamba, Gerardo</creator><creator>Sánchez-Navarro, Andrea</creator><creator>Bobadilla, Norma A</creator><general>MDPI AG</general><general>MDPI</general><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>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>COVID</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/0000-0002-4378-9043</orcidid><orcidid>https://orcid.org/0000-0003-2344-0319</orcidid><orcidid>https://orcid.org/0000-0002-9171-4206</orcidid><orcidid>https://orcid.org/0000-0003-1060-5567</orcidid><orcidid>https://orcid.org/0000-0001-5671-7770</orcidid></search><sort><creationdate>20230425</creationdate><title>SerpinA3K Deficiency Reduces Oxidative Stress in Acute Kidney Injury</title><author>González-Soria, Isaac ; Soto-Valadez, Axel D ; Martínez-Rojas, Miguel Angel ; Ortega-Trejo, Juan Antonio ; Pérez-Villalva, Rosalba ; Gamba, Gerardo ; Sánchez-Navarro, Andrea ; Bobadilla, Norma A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c480t-1a2968268b34a4a106b868667045090d57316dafd8e2d3c7016ee88a3b8a75c93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Acute Kidney Injury - metabolism</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>BAX protein</topic><topic>Biomarkers</topic><topic>Creatinine</topic><topic>Cytokines</topic><topic>FOXO3 protein</topic><topic>Gene expression</topic><topic>Genotypes</topic><topic>Hypoxia</topic><topic>Injury prevention</topic><topic>Ischemia</topic><topic>Kidney - metabolism</topic><topic>Kidney diseases</topic><topic>Kidneys</topic><topic>Mice</topic><topic>Morphology</topic><topic>Mortality</topic><topic>mRNA</topic><topic>Oxidants</topic><topic>Oxidative Stress</topic><topic>Oxidizing agents</topic><topic>Proteins</topic><topic>Renal function</topic><topic>Renal Insufficiency, Chronic - metabolism</topic><topic>Reperfusion</topic><topic>Reperfusion Injury - metabolism</topic><topic>Severe acute respiratory syndrome coronavirus 2</topic><topic>Vascular endothelial growth factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>González-Soria, Isaac</creatorcontrib><creatorcontrib>Soto-Valadez, Axel D</creatorcontrib><creatorcontrib>Martínez-Rojas, Miguel Angel</creatorcontrib><creatorcontrib>Ortega-Trejo, Juan Antonio</creatorcontrib><creatorcontrib>Pérez-Villalva, Rosalba</creatorcontrib><creatorcontrib>Gamba, Gerardo</creatorcontrib><creatorcontrib>Sánchez-Navarro, Andrea</creatorcontrib><creatorcontrib>Bobadilla, Norma A</creatorcontrib><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</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>Coronavirus Research Database</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</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><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>González-Soria, Isaac</au><au>Soto-Valadez, Axel D</au><au>Martínez-Rojas, Miguel Angel</au><au>Ortega-Trejo, Juan Antonio</au><au>Pérez-Villalva, Rosalba</au><au>Gamba, Gerardo</au><au>Sánchez-Navarro, Andrea</au><au>Bobadilla, Norma A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SerpinA3K Deficiency Reduces Oxidative Stress in Acute Kidney Injury</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2023-04-25</date><risdate>2023</risdate><volume>24</volume><issue>9</issue><spage>7815</spage><pages>7815-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>We previously showed that SerpinA3K is present in urine from rats and humans with acute kidney injury (AKI) and chronic kidney disease (CKD). However, the specific role of SerpinA3K during renal pathophysiology is unknown. To begin to understand the role of SerpinA3K on AKI, SerpinA3K-deficient (KOSA3) mice were studied 24 h after inducing ischemia/reperfusion (I/R) and compared to wild type (WT) mice. Four groups were studied: WT+S, WT+IR, KOSA3+S, and KOSA3+IR. As expected, I/R increased serum creatinine and BUN, with a GFR reduction in both genotypes; however, renal dysfunction was ameliorated in the KOSA3+IR group. Interestingly, the increase in UH
O
induced by I/R was not equally seen in the KOSA3+IR group, an effect that was associated with the preservation of antioxidant enzymes' mRNA levels. Additionally, FOXO3 expression was initially greater in the KOSA3 than in the WT group. Moreover, the increase in BAX protein level and the decrease in
and
induced by I/R were not observed in the KOSA3+IR group, suggesting that these animals have better cellular responses to hypoxic injury. Our findings suggest that SerpinA3K is involved in the renal oxidant response, HIF1α/VEGF pathway, and cell apoptosis.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>37175519</pmid><doi>10.3390/ijms24097815</doi><orcidid>https://orcid.org/0000-0002-4378-9043</orcidid><orcidid>https://orcid.org/0000-0003-2344-0319</orcidid><orcidid>https://orcid.org/0000-0002-9171-4206</orcidid><orcidid>https://orcid.org/0000-0003-1060-5567</orcidid><orcidid>https://orcid.org/0000-0001-5671-7770</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Acute Kidney Injury - metabolism Animals Apoptosis BAX protein Biomarkers Creatinine Cytokines FOXO3 protein Gene expression Genotypes Hypoxia Injury prevention Ischemia Kidney - metabolism Kidney diseases Kidneys Mice Morphology Mortality mRNA Oxidants Oxidative Stress Oxidizing agents Proteins Renal function Renal Insufficiency, Chronic - metabolism Reperfusion Reperfusion Injury - metabolism Severe acute respiratory syndrome coronavirus 2 Vascular endothelial growth factor |
| title | SerpinA3K Deficiency Reduces Oxidative Stress in Acute Kidney Injury |
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