MicroRNA-21 Attenuates Renal Ischemia Reperfusion Injury via Targeting Caspase Signaling in Mice
Background: MicroRNAs (miR) have come into focus as powerful regulators of gene expression and potential diagnostic tools during renal ischemia reperfusion injury (IRI). The aim of this study was to investigate the molecular regulation and function of miR-21, and to analyze the relationship between...
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| Veröffentlicht in: | American journal of nephrology 2014-01, Vol.40 (3), p.215-223 |
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| creator | Hu, Honglin Jiang, Wei Xi, Xiaoqing Zou, Cong Ye, Zhenfeng |
| description | Background: MicroRNAs (miR) have come into focus as powerful regulators of gene expression and potential diagnostic tools during renal ischemia reperfusion injury (IRI). The aim of this study was to investigate the molecular regulation and function of miR-21, and to analyze the relationship between caspases and miR-21 expression levels in an experimental model of renal IRI. Methods: IRI was induced by bilateral renal ischemia for 45 min followed by reperfusion. The male BALB/c mice were randomly assigned to the following groups: pre-miR-21 + IRI group, antagomiR-21 + IRI group, PBS + IRI group, pre-miR-21 + sham operation group, antagomiR-21 + sham operation group, PBS + sham operation group. The pre-miR-21 or antagomiR-21 was administered intraperitoneally (200 ng/kg weight) 24 and 6 h before induction of ischemia. Renal function, histological damage, renal cell apoptosis proteins were evaluated at 24 h after reperfusion. Results: Mice upregulated miR-21 had lower plasma levels of blood urea nitrogen (BUN) and creatinine, lower histopathological scores and a decrease in programmed cell death 4 (PDCD4) mRNA and active caspase-3, caspase-8 proteins expressions. Conclusions: miR-21 is endowed with anti-apoptotic properties by suppressing the expression of PDCD4 gene and active caspase 3/8 fragments in the condition of renal IRI. miR-21 exerts significant functional protection in our renal murine model of IRI. |
| doi_str_mv | 10.1159/000368202 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_1627113497</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3505605941</sourcerecordid><originalsourceid>FETCH-LOGICAL-c400t-f41f204e8cc9ec2f90cf864e53857ba5730c9a7593d620dead90f359c1cdc0673</originalsourceid><addsrcrecordid>eNpdkE1Lw0AQhhdRbK0evIsEvOghOrubTbLHUvwoVIVaz3G7mdTUfLmbCP33bmjtwdMww_O-DA8h5xRuKRXyDgB4GDNgB2RIA0Z9GUZwSIbABPgxSDEgJ9auASiLITomAyY4Y6HkQ_LxnGtTz1_GPqPeuG2x6lSL1ptjpQpvavUnlrlya4Mm62xeV960Wndm4_2480KZFbZ5tfImyjbKoveWr1ywv-SV57rxlBxlqrB4tpsj8v5wv5g8-bPXx-lkPPN1AND6WUAzBgHGWkvULJOgszgMUPBYREslIg5aqkhInoYMUlSphIwLqalONYQRH5HrbW9j6u8ObZuUudVYFKrCurMJDankjAYhc-jVP3Rdd8a93VMsopQHsi-82VLOj7UGs6QxeanMJqGQ9NqTvXbHXu4au2WJ6Z788-yAiy3w1Rsze2CX_wXCb4Py</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1627113497</pqid></control><display><type>article</type><title>MicroRNA-21 Attenuates Renal Ischemia Reperfusion Injury via Targeting Caspase Signaling in Mice</title><source>MEDLINE</source><source>Karger Journals</source><creator>Hu, Honglin ; Jiang, Wei ; Xi, Xiaoqing ; Zou, Cong ; Ye, Zhenfeng</creator><creatorcontrib>Hu, Honglin ; Jiang, Wei ; Xi, Xiaoqing ; Zou, Cong ; Ye, Zhenfeng</creatorcontrib><description>Background: MicroRNAs (miR) have come into focus as powerful regulators of gene expression and potential diagnostic tools during renal ischemia reperfusion injury (IRI). The aim of this study was to investigate the molecular regulation and function of miR-21, and to analyze the relationship between caspases and miR-21 expression levels in an experimental model of renal IRI. Methods: IRI was induced by bilateral renal ischemia for 45 min followed by reperfusion. The male BALB/c mice were randomly assigned to the following groups: pre-miR-21 + IRI group, antagomiR-21 + IRI group, PBS + IRI group, pre-miR-21 + sham operation group, antagomiR-21 + sham operation group, PBS + sham operation group. The pre-miR-21 or antagomiR-21 was administered intraperitoneally (200 ng/kg weight) 24 and 6 h before induction of ischemia. Renal function, histological damage, renal cell apoptosis proteins were evaluated at 24 h after reperfusion. Results: Mice upregulated miR-21 had lower plasma levels of blood urea nitrogen (BUN) and creatinine, lower histopathological scores and a decrease in programmed cell death 4 (PDCD4) mRNA and active caspase-3, caspase-8 proteins expressions. Conclusions: miR-21 is endowed with anti-apoptotic properties by suppressing the expression of PDCD4 gene and active caspase 3/8 fragments in the condition of renal IRI. miR-21 exerts significant functional protection in our renal murine model of IRI.</description><identifier>ISSN: 0250-8095</identifier><identifier>EISSN: 1421-9670</identifier><identifier>DOI: 10.1159/000368202</identifier><identifier>PMID: 25322693</identifier><identifier>CODEN: AJNED9</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Animals ; Apoptosis ; Apoptosis Regulatory Proteins - metabolism ; Blood Urea Nitrogen ; Caspase 3 - metabolism ; Caspase 8 - metabolism ; Caspases - metabolism ; Disease Models, Animal ; Gene Expression Profiling ; Interleukin-18 - blood ; Ischemia - metabolism ; Kidney - metabolism ; Kidney - pathology ; Male ; Mice ; Mice, Inbred BALB C ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Original Report: Laboratory Investigation ; Random Allocation ; Reperfusion Injury - pathology ; RNA-Binding Proteins - metabolism ; Signal Transduction ; Up-Regulation</subject><ispartof>American journal of nephrology, 2014-01, Vol.40 (3), p.215-223</ispartof><rights>2014 S. Karger AG, Basel</rights><rights>2014 S. Karger AG, Basel.</rights><rights>Copyright (c) 2014 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c400t-f41f204e8cc9ec2f90cf864e53857ba5730c9a7593d620dead90f359c1cdc0673</citedby><cites>FETCH-LOGICAL-c400t-f41f204e8cc9ec2f90cf864e53857ba5730c9a7593d620dead90f359c1cdc0673</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2428,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25322693$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hu, Honglin</creatorcontrib><creatorcontrib>Jiang, Wei</creatorcontrib><creatorcontrib>Xi, Xiaoqing</creatorcontrib><creatorcontrib>Zou, Cong</creatorcontrib><creatorcontrib>Ye, Zhenfeng</creatorcontrib><title>MicroRNA-21 Attenuates Renal Ischemia Reperfusion Injury via Targeting Caspase Signaling in Mice</title><title>American journal of nephrology</title><addtitle>Am J Nephrol</addtitle><description>Background: MicroRNAs (miR) have come into focus as powerful regulators of gene expression and potential diagnostic tools during renal ischemia reperfusion injury (IRI). The aim of this study was to investigate the molecular regulation and function of miR-21, and to analyze the relationship between caspases and miR-21 expression levels in an experimental model of renal IRI. Methods: IRI was induced by bilateral renal ischemia for 45 min followed by reperfusion. The male BALB/c mice were randomly assigned to the following groups: pre-miR-21 + IRI group, antagomiR-21 + IRI group, PBS + IRI group, pre-miR-21 + sham operation group, antagomiR-21 + sham operation group, PBS + sham operation group. The pre-miR-21 or antagomiR-21 was administered intraperitoneally (200 ng/kg weight) 24 and 6 h before induction of ischemia. Renal function, histological damage, renal cell apoptosis proteins were evaluated at 24 h after reperfusion. Results: Mice upregulated miR-21 had lower plasma levels of blood urea nitrogen (BUN) and creatinine, lower histopathological scores and a decrease in programmed cell death 4 (PDCD4) mRNA and active caspase-3, caspase-8 proteins expressions. Conclusions: miR-21 is endowed with anti-apoptotic properties by suppressing the expression of PDCD4 gene and active caspase 3/8 fragments in the condition of renal IRI. miR-21 exerts significant functional protection in our renal murine model of IRI.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Blood Urea Nitrogen</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase 8 - metabolism</subject><subject>Caspases - metabolism</subject><subject>Disease Models, Animal</subject><subject>Gene Expression Profiling</subject><subject>Interleukin-18 - blood</subject><subject>Ischemia - metabolism</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Original Report: Laboratory Investigation</subject><subject>Random Allocation</subject><subject>Reperfusion Injury - pathology</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Signal Transduction</subject><subject>Up-Regulation</subject><issn>0250-8095</issn><issn>1421-9670</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</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>eNpdkE1Lw0AQhhdRbK0evIsEvOghOrubTbLHUvwoVIVaz3G7mdTUfLmbCP33bmjtwdMww_O-DA8h5xRuKRXyDgB4GDNgB2RIA0Z9GUZwSIbABPgxSDEgJ9auASiLITomAyY4Y6HkQ_LxnGtTz1_GPqPeuG2x6lSL1ptjpQpvavUnlrlya4Mm62xeV960Wndm4_2480KZFbZ5tfImyjbKoveWr1ywv-SV57rxlBxlqrB4tpsj8v5wv5g8-bPXx-lkPPN1AND6WUAzBgHGWkvULJOgszgMUPBYREslIg5aqkhInoYMUlSphIwLqalONYQRH5HrbW9j6u8ObZuUudVYFKrCurMJDankjAYhc-jVP3Rdd8a93VMsopQHsi-82VLOj7UGs6QxeanMJqGQ9NqTvXbHXu4au2WJ6Z788-yAiy3w1Rsze2CX_wXCb4Py</recordid><startdate>20140101</startdate><enddate>20140101</enddate><creator>Hu, Honglin</creator><creator>Jiang, Wei</creator><creator>Xi, Xiaoqing</creator><creator>Zou, Cong</creator><creator>Ye, Zhenfeng</creator><general>S. Karger AG</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>7QL</scope><scope>7QP</scope><scope>7RV</scope><scope>7T7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</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>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope></search><sort><creationdate>20140101</creationdate><title>MicroRNA-21 Attenuates Renal Ischemia Reperfusion Injury via Targeting Caspase Signaling in Mice</title><author>Hu, Honglin ; Jiang, Wei ; Xi, Xiaoqing ; Zou, Cong ; Ye, Zhenfeng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c400t-f41f204e8cc9ec2f90cf864e53857ba5730c9a7593d620dead90f359c1cdc0673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Blood Urea Nitrogen</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase 8 - metabolism</topic><topic>Caspases - metabolism</topic><topic>Disease Models, Animal</topic><topic>Gene Expression Profiling</topic><topic>Interleukin-18 - blood</topic><topic>Ischemia - metabolism</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Original Report: Laboratory Investigation</topic><topic>Random Allocation</topic><topic>Reperfusion Injury - pathology</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Signal Transduction</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Honglin</creatorcontrib><creatorcontrib>Jiang, Wei</creatorcontrib><creatorcontrib>Xi, Xiaoqing</creatorcontrib><creatorcontrib>Zou, Cong</creatorcontrib><creatorcontrib>Ye, Zhenfeng</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</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>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of nephrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Honglin</au><au>Jiang, Wei</au><au>Xi, Xiaoqing</au><au>Zou, Cong</au><au>Ye, Zhenfeng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA-21 Attenuates Renal Ischemia Reperfusion Injury via Targeting Caspase Signaling in Mice</atitle><jtitle>American journal of nephrology</jtitle><addtitle>Am J Nephrol</addtitle><date>2014-01-01</date><risdate>2014</risdate><volume>40</volume><issue>3</issue><spage>215</spage><epage>223</epage><pages>215-223</pages><issn>0250-8095</issn><eissn>1421-9670</eissn><coden>AJNED9</coden><abstract>Background: MicroRNAs (miR) have come into focus as powerful regulators of gene expression and potential diagnostic tools during renal ischemia reperfusion injury (IRI). The aim of this study was to investigate the molecular regulation and function of miR-21, and to analyze the relationship between caspases and miR-21 expression levels in an experimental model of renal IRI. Methods: IRI was induced by bilateral renal ischemia for 45 min followed by reperfusion. The male BALB/c mice were randomly assigned to the following groups: pre-miR-21 + IRI group, antagomiR-21 + IRI group, PBS + IRI group, pre-miR-21 + sham operation group, antagomiR-21 + sham operation group, PBS + sham operation group. The pre-miR-21 or antagomiR-21 was administered intraperitoneally (200 ng/kg weight) 24 and 6 h before induction of ischemia. Renal function, histological damage, renal cell apoptosis proteins were evaluated at 24 h after reperfusion. Results: Mice upregulated miR-21 had lower plasma levels of blood urea nitrogen (BUN) and creatinine, lower histopathological scores and a decrease in programmed cell death 4 (PDCD4) mRNA and active caspase-3, caspase-8 proteins expressions. Conclusions: miR-21 is endowed with anti-apoptotic properties by suppressing the expression of PDCD4 gene and active caspase 3/8 fragments in the condition of renal IRI. miR-21 exerts significant functional protection in our renal murine model of IRI.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>25322693</pmid><doi>10.1159/000368202</doi><tpages>9</tpages></addata></record> |
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| subjects | Animals Apoptosis Apoptosis Regulatory Proteins - metabolism Blood Urea Nitrogen Caspase 3 - metabolism Caspase 8 - metabolism Caspases - metabolism Disease Models, Animal Gene Expression Profiling Interleukin-18 - blood Ischemia - metabolism Kidney - metabolism Kidney - pathology Male Mice Mice, Inbred BALB C MicroRNAs - genetics MicroRNAs - metabolism Original Report: Laboratory Investigation Random Allocation Reperfusion Injury - pathology RNA-Binding Proteins - metabolism Signal Transduction Up-Regulation |
| title | MicroRNA-21 Attenuates Renal Ischemia Reperfusion Injury via Targeting Caspase Signaling in Mice |
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