Modification of cardiac thyroid hormone deiodinases expression in an ischemia/reperfusion rat model after T3 infusion
The deiodinases regulate the activation and inactivation of Thyroid hormones (TH), in both physiological and pathological conditions. The three deiodinases, DIO1, DIO2 and DIO3, have different catalytic role and cellular and tissue distribution. Aim of this study is to evaluate a rat model of region...
Gespeichert in:
Veröffentlicht in: | Molecular and cellular biochemistry 2020-12, Vol.475 (1-2), p.205-214 |
---|---|
Hauptverfasser: | , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 214 |
---|---|
container_issue | 1-2 |
container_start_page | 205 |
container_title | Molecular and cellular biochemistry |
container_volume | 475 |
creator | Sabatino, Laura Kusmic, Claudia Iervasi, Giorgio |
description | The deiodinases regulate the activation and inactivation of Thyroid hormones (TH), in both physiological and pathological conditions. The three deiodinases, DIO1, DIO2 and DIO3, have different catalytic role and cellular and tissue distribution. Aim of this study is to evaluate a rat model of regional ischemia/reperfusion (I/R), the modification of cardiac main function after the administration of 6 µg/kg/day of triiodothyronine (T3), and the associated to DIO1, DIO2 and DIO3 gene expression. We also aim to study DIO1 and DIO2 protein levels in different left ventricular regions after an ischemic event. Four groups of rats were studied: sham-operated, sham-operated + T3, I/R rats and I/R rats + T3. DIO1, DIO2 and DIO3 expression were evaluated in I/R region (AAR: area-at-risk) and in a more distant region from ischemic wound (RZ: remote zone). In I/R group, circulating free-T3 (FT3) levels were significantly decreased with respect to basal values, whereas in I/R + T3 rats, FT3 levels were comparable to basal values. In AAR of I/R + T3 rats, DIO1 and DIO2 gene expression significantly increased with respect to sham. In RZ, DIO1 and DIO3 gene expression was significantly lower in sham and I/R rats when compared to I/R + T3. In sham + T3 group, DIO1 and DIO2 gene expression was not detectable, whereas DIO3 was significantly higher than in the other three groups. The present study gives interesting new insights on DIO1, DIO2 and DIO3 in the ischemic heart and their role in relation to T3-mediated amelioration of cardiac function and structure. |
doi_str_mv | 10.1007/s11010-020-03873-w |
format | Article |
fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_2432860588</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A640045707</galeid><sourcerecordid>A640045707</sourcerecordid><originalsourceid>FETCH-LOGICAL-c419t-644fa172d774fd68a0d594980d621eeaf49ba953e9bb730956b5364ebcecd543</originalsourceid><addsrcrecordid>eNp9kcFq3DAQhkVpodu0L9CToJdenIws2bKPIbRpISGXvQtZGmUVbGsr2aR5-87GhdBSipBGaL5_GM3P2EcB5wJAXxQhQEAFNW3ZaVk9vmI70dBF9aJ_zXYgAapOaP2WvSvlAYgGIXZsvU0-hujsEtPMU-DOZh-t48vhKafo-SHlKc3IPUYiZ1uwcPx5zFjKSRFnbuks7oBTtBcZj5jD-pzKduFT8jhyGxbMfC-J3nLv2Ztgx4Iffscztv_6ZX_1rbq5u_5-dXlTOSX6pWqVClbo2mutgm87C77pVd-Bb2uBaIPqB9s3Evth0BL6ph0a2SocHDrfKHnGPm9ljzn9WLEsZqJOcRztjGktplay7lpouo7QT3-hD2nNMzVHlBaNVG0LL9S9HdHQb9KSrTsVNZetAlCNBk3U-T8oWp5m5GiYIdL7H4J6E7icSskYzDHHyeYnI8Cc_DWbv4b8Nc_-mkcSyU1UCJ7vMb90_B_VL5Q1qJk</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2471534660</pqid></control><display><type>article</type><title>Modification of cardiac thyroid hormone deiodinases expression in an ischemia/reperfusion rat model after T3 infusion</title><source>SpringerLink Journals - AutoHoldings</source><creator>Sabatino, Laura ; Kusmic, Claudia ; Iervasi, Giorgio</creator><creatorcontrib>Sabatino, Laura ; Kusmic, Claudia ; Iervasi, Giorgio</creatorcontrib><description>The deiodinases regulate the activation and inactivation of Thyroid hormones (TH), in both physiological and pathological conditions. The three deiodinases, DIO1, DIO2 and DIO3, have different catalytic role and cellular and tissue distribution. Aim of this study is to evaluate a rat model of regional ischemia/reperfusion (I/R), the modification of cardiac main function after the administration of 6 µg/kg/day of triiodothyronine (T3), and the associated to DIO1, DIO2 and DIO3 gene expression. We also aim to study DIO1 and DIO2 protein levels in different left ventricular regions after an ischemic event. Four groups of rats were studied: sham-operated, sham-operated + T3, I/R rats and I/R rats + T3. DIO1, DIO2 and DIO3 expression were evaluated in I/R region (AAR: area-at-risk) and in a more distant region from ischemic wound (RZ: remote zone). In I/R group, circulating free-T3 (FT3) levels were significantly decreased with respect to basal values, whereas in I/R + T3 rats, FT3 levels were comparable to basal values. In AAR of I/R + T3 rats, DIO1 and DIO2 gene expression significantly increased with respect to sham. In RZ, DIO1 and DIO3 gene expression was significantly lower in sham and I/R rats when compared to I/R + T3. In sham + T3 group, DIO1 and DIO2 gene expression was not detectable, whereas DIO3 was significantly higher than in the other three groups. The present study gives interesting new insights on DIO1, DIO2 and DIO3 in the ischemic heart and their role in relation to T3-mediated amelioration of cardiac function and structure.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-020-03873-w</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Biochemistry ; Biomedical and Life Sciences ; Cardiology ; Gene expression ; Heart ; Hormones ; Inactivation ; Ischemia ; Life Sciences ; Mediation ; Medical Biochemistry ; Oncology ; Reperfusion ; Rodents ; Structure-function relationships ; Thyroid ; Thyroid gland ; Thyroid hormones ; Thyroxine deiodinase ; Triiodothyronine ; Ventricle</subject><ispartof>Molecular and cellular biochemistry, 2020-12, Vol.475 (1-2), p.205-214</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>COPYRIGHT 2020 Springer</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-644fa172d774fd68a0d594980d621eeaf49ba953e9bb730956b5364ebcecd543</citedby><cites>FETCH-LOGICAL-c419t-644fa172d774fd68a0d594980d621eeaf49ba953e9bb730956b5364ebcecd543</cites><orcidid>0000-0002-9283-5042</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-020-03873-w$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-020-03873-w$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids></links><search><creatorcontrib>Sabatino, Laura</creatorcontrib><creatorcontrib>Kusmic, Claudia</creatorcontrib><creatorcontrib>Iervasi, Giorgio</creatorcontrib><title>Modification of cardiac thyroid hormone deiodinases expression in an ischemia/reperfusion rat model after T3 infusion</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><description>The deiodinases regulate the activation and inactivation of Thyroid hormones (TH), in both physiological and pathological conditions. The three deiodinases, DIO1, DIO2 and DIO3, have different catalytic role and cellular and tissue distribution. Aim of this study is to evaluate a rat model of regional ischemia/reperfusion (I/R), the modification of cardiac main function after the administration of 6 µg/kg/day of triiodothyronine (T3), and the associated to DIO1, DIO2 and DIO3 gene expression. We also aim to study DIO1 and DIO2 protein levels in different left ventricular regions after an ischemic event. Four groups of rats were studied: sham-operated, sham-operated + T3, I/R rats and I/R rats + T3. DIO1, DIO2 and DIO3 expression were evaluated in I/R region (AAR: area-at-risk) and in a more distant region from ischemic wound (RZ: remote zone). In I/R group, circulating free-T3 (FT3) levels were significantly decreased with respect to basal values, whereas in I/R + T3 rats, FT3 levels were comparable to basal values. In AAR of I/R + T3 rats, DIO1 and DIO2 gene expression significantly increased with respect to sham. In RZ, DIO1 and DIO3 gene expression was significantly lower in sham and I/R rats when compared to I/R + T3. In sham + T3 group, DIO1 and DIO2 gene expression was not detectable, whereas DIO3 was significantly higher than in the other three groups. The present study gives interesting new insights on DIO1, DIO2 and DIO3 in the ischemic heart and their role in relation to T3-mediated amelioration of cardiac function and structure.</description><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiology</subject><subject>Gene expression</subject><subject>Heart</subject><subject>Hormones</subject><subject>Inactivation</subject><subject>Ischemia</subject><subject>Life Sciences</subject><subject>Mediation</subject><subject>Medical Biochemistry</subject><subject>Oncology</subject><subject>Reperfusion</subject><subject>Rodents</subject><subject>Structure-function relationships</subject><subject>Thyroid</subject><subject>Thyroid gland</subject><subject>Thyroid hormones</subject><subject>Thyroxine deiodinase</subject><subject>Triiodothyronine</subject><subject>Ventricle</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kcFq3DAQhkVpodu0L9CToJdenIws2bKPIbRpISGXvQtZGmUVbGsr2aR5-87GhdBSipBGaL5_GM3P2EcB5wJAXxQhQEAFNW3ZaVk9vmI70dBF9aJ_zXYgAapOaP2WvSvlAYgGIXZsvU0-hujsEtPMU-DOZh-t48vhKafo-SHlKc3IPUYiZ1uwcPx5zFjKSRFnbuks7oBTtBcZj5jD-pzKduFT8jhyGxbMfC-J3nLv2Ztgx4Iffscztv_6ZX_1rbq5u_5-dXlTOSX6pWqVClbo2mutgm87C77pVd-Bb2uBaIPqB9s3Evth0BL6ph0a2SocHDrfKHnGPm9ljzn9WLEsZqJOcRztjGktplay7lpouo7QT3-hD2nNMzVHlBaNVG0LL9S9HdHQb9KSrTsVNZetAlCNBk3U-T8oWp5m5GiYIdL7H4J6E7icSskYzDHHyeYnI8Cc_DWbv4b8Nc_-mkcSyU1UCJ7vMb90_B_VL5Q1qJk</recordid><startdate>20201201</startdate><enddate>20201201</enddate><creator>Sabatino, Laura</creator><creator>Kusmic, Claudia</creator><creator>Iervasi, Giorgio</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</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>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-9283-5042</orcidid></search><sort><creationdate>20201201</creationdate><title>Modification of cardiac thyroid hormone deiodinases expression in an ischemia/reperfusion rat model after T3 infusion</title><author>Sabatino, Laura ; Kusmic, Claudia ; Iervasi, Giorgio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-644fa172d774fd68a0d594980d621eeaf49ba953e9bb730956b5364ebcecd543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cardiology</topic><topic>Gene expression</topic><topic>Heart</topic><topic>Hormones</topic><topic>Inactivation</topic><topic>Ischemia</topic><topic>Life Sciences</topic><topic>Mediation</topic><topic>Medical Biochemistry</topic><topic>Oncology</topic><topic>Reperfusion</topic><topic>Rodents</topic><topic>Structure-function relationships</topic><topic>Thyroid</topic><topic>Thyroid gland</topic><topic>Thyroid hormones</topic><topic>Thyroxine deiodinase</topic><topic>Triiodothyronine</topic><topic>Ventricle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sabatino, Laura</creatorcontrib><creatorcontrib>Kusmic, Claudia</creatorcontrib><creatorcontrib>Iervasi, Giorgio</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</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>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database (ProQuest)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</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 Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sabatino, Laura</au><au>Kusmic, Claudia</au><au>Iervasi, Giorgio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modification of cardiac thyroid hormone deiodinases expression in an ischemia/reperfusion rat model after T3 infusion</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><date>2020-12-01</date><risdate>2020</risdate><volume>475</volume><issue>1-2</issue><spage>205</spage><epage>214</epage><pages>205-214</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>The deiodinases regulate the activation and inactivation of Thyroid hormones (TH), in both physiological and pathological conditions. The three deiodinases, DIO1, DIO2 and DIO3, have different catalytic role and cellular and tissue distribution. Aim of this study is to evaluate a rat model of regional ischemia/reperfusion (I/R), the modification of cardiac main function after the administration of 6 µg/kg/day of triiodothyronine (T3), and the associated to DIO1, DIO2 and DIO3 gene expression. We also aim to study DIO1 and DIO2 protein levels in different left ventricular regions after an ischemic event. Four groups of rats were studied: sham-operated, sham-operated + T3, I/R rats and I/R rats + T3. DIO1, DIO2 and DIO3 expression were evaluated in I/R region (AAR: area-at-risk) and in a more distant region from ischemic wound (RZ: remote zone). In I/R group, circulating free-T3 (FT3) levels were significantly decreased with respect to basal values, whereas in I/R + T3 rats, FT3 levels were comparable to basal values. In AAR of I/R + T3 rats, DIO1 and DIO2 gene expression significantly increased with respect to sham. In RZ, DIO1 and DIO3 gene expression was significantly lower in sham and I/R rats when compared to I/R + T3. In sham + T3 group, DIO1 and DIO2 gene expression was not detectable, whereas DIO3 was significantly higher than in the other three groups. The present study gives interesting new insights on DIO1, DIO2 and DIO3 in the ischemic heart and their role in relation to T3-mediated amelioration of cardiac function and structure.</abstract><cop>New York</cop><pub>Springer US</pub><doi>10.1007/s11010-020-03873-w</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-9283-5042</orcidid></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0300-8177 |
ispartof | Molecular and cellular biochemistry, 2020-12, Vol.475 (1-2), p.205-214 |
issn | 0300-8177 1573-4919 |
language | eng |
recordid | cdi_proquest_miscellaneous_2432860588 |
source | SpringerLink Journals - AutoHoldings |
subjects | Biochemistry Biomedical and Life Sciences Cardiology Gene expression Heart Hormones Inactivation Ischemia Life Sciences Mediation Medical Biochemistry Oncology Reperfusion Rodents Structure-function relationships Thyroid Thyroid gland Thyroid hormones Thyroxine deiodinase Triiodothyronine Ventricle |
title | Modification of cardiac thyroid hormone deiodinases expression in an ischemia/reperfusion rat model after T3 infusion |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-09T08%3A05%3A29IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Modification%20of%20cardiac%20thyroid%20hormone%20deiodinases%20expression%20in%20an%20ischemia/reperfusion%20rat%20model%20after%20T3%20infusion&rft.jtitle=Molecular%20and%20cellular%20biochemistry&rft.au=Sabatino,%20Laura&rft.date=2020-12-01&rft.volume=475&rft.issue=1-2&rft.spage=205&rft.epage=214&rft.pages=205-214&rft.issn=0300-8177&rft.eissn=1573-4919&rft_id=info:doi/10.1007/s11010-020-03873-w&rft_dat=%3Cgale_proqu%3EA640045707%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2471534660&rft_id=info:pmid/&rft_galeid=A640045707&rfr_iscdi=true |