Cardiomyocytic FoxP3 is involved in Parkin-mediated mitophagy during cardiac remodeling and the regulatory role of triptolide
Forkhead/winged helix transcriptional factor P3 (FoxP3) is a well-studied transcription factor that maintains the activity of T cells, but whether cardiomyocytic FoxP3 participates in cardiac remodeling (CR) remains unclear. The present study was to investigate the role of cardiomyocytic FoxP3 in CR...
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| Veröffentlicht in: | Theranostics 2022-01, Vol.12 (5), p.2483-2501 |
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| creator | Pan, Xi-Chun Xiong, Ya-Lan Hong, Jia-Hui Liu, Ya Cen, Yan-Yan Liu, Tao Yang, Qun-Fang Tao, Hui Li, Yu-Nong Zhang, Hai-Gang |
| description | Forkhead/winged helix transcriptional factor P3 (FoxP3) is a well-studied transcription factor that maintains the activity of T cells, but whether cardiomyocytic FoxP3 participates in cardiac remodeling (CR) remains unclear. The present study was to investigate the role of cardiomyocytic FoxP3 in CR from the perspective of mitophagy.
CR was induced by angiotensin II (AngII)
, or by isoproterenol (Iso)
using male C57 mice or FoxP3
mice. Histological changes were observed by hematoxylin-eosin and Masson staining. Molecular changes were detected by immunohistochemistry, immunofluorescence, immunoblotting, and real-time PCR. Mitophagy was shaped by transmission electron microscopy and co-localization. The mRNA expression was operated by siRNA or adeno associated virus (AAV). Molecular interactions were detected by co-localization, immunoprecipitation (IP), and chromatin IP.
The expression and nuclear translocation of cardiomyocytic FoxP3 were downregulated in CR, while they were upregulated after triptolide (TP) treatment. In left ventricle (LV) remodeling in mice, autophagy was activated continuously in the myocardium, and TP significantly attenuated it. AngII induced massive mitophagy characterized by the activation of autophagy regulatory protein 5 (Atg5)-dependent autophagic flux. Critically, Parkin was identified as the main adaptor mediated myocardial mitophagy and was responsible for the effect of TP. Moreover, FoxP3 was responsible for the downregulation of Parkin and inhibited AngII-induced cardiac mitophagy. We found that mitophagy increased significantly and the inhibition of TP treatment reversed completely in FoxP3-deficient LVs. Mechanistically, FoxP3 interacted with a motif located downstream of the activating transcription 4 (ATF4)-binding motif involved in the promoter of
and hijacked free nuclear ATF4 to decrease
mRNA expression in CR.
Cardiomyocytic FoxP3 could negatively regulate Parkin-mediated mitophagy in CR, and restoring cardiomyocytic FoxP3 activity provided a cardioprotective strategy by inhibiting excessive cardiac mitophagy. |
| doi_str_mv | 10.7150/thno.71102 |
| format | Article |
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CR was induced by angiotensin II (AngII)
, or by isoproterenol (Iso)
using male C57 mice or FoxP3
mice. Histological changes were observed by hematoxylin-eosin and Masson staining. Molecular changes were detected by immunohistochemistry, immunofluorescence, immunoblotting, and real-time PCR. Mitophagy was shaped by transmission electron microscopy and co-localization. The mRNA expression was operated by siRNA or adeno associated virus (AAV). Molecular interactions were detected by co-localization, immunoprecipitation (IP), and chromatin IP.
The expression and nuclear translocation of cardiomyocytic FoxP3 were downregulated in CR, while they were upregulated after triptolide (TP) treatment. In left ventricle (LV) remodeling in mice, autophagy was activated continuously in the myocardium, and TP significantly attenuated it. AngII induced massive mitophagy characterized by the activation of autophagy regulatory protein 5 (Atg5)-dependent autophagic flux. Critically, Parkin was identified as the main adaptor mediated myocardial mitophagy and was responsible for the effect of TP. Moreover, FoxP3 was responsible for the downregulation of Parkin and inhibited AngII-induced cardiac mitophagy. We found that mitophagy increased significantly and the inhibition of TP treatment reversed completely in FoxP3-deficient LVs. Mechanistically, FoxP3 interacted with a motif located downstream of the activating transcription 4 (ATF4)-binding motif involved in the promoter of
and hijacked free nuclear ATF4 to decrease
mRNA expression in CR.
Cardiomyocytic FoxP3 could negatively regulate Parkin-mediated mitophagy in CR, and restoring cardiomyocytic FoxP3 activity provided a cardioprotective strategy by inhibiting excessive cardiac mitophagy.</description><identifier>ISSN: 1838-7640</identifier><identifier>EISSN: 1838-7640</identifier><identifier>DOI: 10.7150/thno.71102</identifier><identifier>PMID: 35265221</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher Pty Ltd</publisher><subject>Angiotensin II - pharmacology ; Animals ; Antibodies ; Autophagy ; Cardiomyocytes ; Diterpenes ; Epoxy Compounds ; Forkhead Transcription Factors - metabolism ; Heart ; Kinases ; Laboratory animals ; Male ; Mice ; Mitochondria ; Mitochondria - metabolism ; Mitophagy - genetics ; Phenanthrenes ; Proteins ; Reagents ; Research Paper ; RNA, Messenger - metabolism ; Ubiquitin-Protein Ligases - metabolism ; Ventricular Remodeling</subject><ispartof>Theranostics, 2022-01, Vol.12 (5), p.2483-2501</ispartof><rights>The author(s).</rights><rights>2022. This work is published under https://creativecommons.org/licenses/by/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>The author(s) 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c406t-88ba79ab19dc254b75ea08b6b74e8a8a3b931ef71ea459f3e06f02331708ba033</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8899572/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8899572/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35265221$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pan, Xi-Chun</creatorcontrib><creatorcontrib>Xiong, Ya-Lan</creatorcontrib><creatorcontrib>Hong, Jia-Hui</creatorcontrib><creatorcontrib>Liu, Ya</creatorcontrib><creatorcontrib>Cen, Yan-Yan</creatorcontrib><creatorcontrib>Liu, Tao</creatorcontrib><creatorcontrib>Yang, Qun-Fang</creatorcontrib><creatorcontrib>Tao, Hui</creatorcontrib><creatorcontrib>Li, Yu-Nong</creatorcontrib><creatorcontrib>Zhang, Hai-Gang</creatorcontrib><title>Cardiomyocytic FoxP3 is involved in Parkin-mediated mitophagy during cardiac remodeling and the regulatory role of triptolide</title><title>Theranostics</title><addtitle>Theranostics</addtitle><description>Forkhead/winged helix transcriptional factor P3 (FoxP3) is a well-studied transcription factor that maintains the activity of T cells, but whether cardiomyocytic FoxP3 participates in cardiac remodeling (CR) remains unclear. The present study was to investigate the role of cardiomyocytic FoxP3 in CR from the perspective of mitophagy.
CR was induced by angiotensin II (AngII)
, or by isoproterenol (Iso)
using male C57 mice or FoxP3
mice. Histological changes were observed by hematoxylin-eosin and Masson staining. Molecular changes were detected by immunohistochemistry, immunofluorescence, immunoblotting, and real-time PCR. Mitophagy was shaped by transmission electron microscopy and co-localization. The mRNA expression was operated by siRNA or adeno associated virus (AAV). Molecular interactions were detected by co-localization, immunoprecipitation (IP), and chromatin IP.
The expression and nuclear translocation of cardiomyocytic FoxP3 were downregulated in CR, while they were upregulated after triptolide (TP) treatment. In left ventricle (LV) remodeling in mice, autophagy was activated continuously in the myocardium, and TP significantly attenuated it. AngII induced massive mitophagy characterized by the activation of autophagy regulatory protein 5 (Atg5)-dependent autophagic flux. Critically, Parkin was identified as the main adaptor mediated myocardial mitophagy and was responsible for the effect of TP. Moreover, FoxP3 was responsible for the downregulation of Parkin and inhibited AngII-induced cardiac mitophagy. We found that mitophagy increased significantly and the inhibition of TP treatment reversed completely in FoxP3-deficient LVs. Mechanistically, FoxP3 interacted with a motif located downstream of the activating transcription 4 (ATF4)-binding motif involved in the promoter of
and hijacked free nuclear ATF4 to decrease
mRNA expression in CR.
Cardiomyocytic FoxP3 could negatively regulate Parkin-mediated mitophagy in CR, and restoring cardiomyocytic FoxP3 activity provided a cardioprotective strategy by inhibiting excessive cardiac mitophagy.</description><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Autophagy</subject><subject>Cardiomyocytes</subject><subject>Diterpenes</subject><subject>Epoxy Compounds</subject><subject>Forkhead Transcription Factors - metabolism</subject><subject>Heart</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>Mice</subject><subject>Mitochondria</subject><subject>Mitochondria - metabolism</subject><subject>Mitophagy - genetics</subject><subject>Phenanthrenes</subject><subject>Proteins</subject><subject>Reagents</subject><subject>Research Paper</subject><subject>RNA, Messenger - metabolism</subject><subject>Ubiquitin-Protein Ligases - metabolism</subject><subject>Ventricular Remodeling</subject><issn>1838-7640</issn><issn>1838-7640</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkc1rFTEUxYMottRu_AMk4EYKo_mYj2QjyMPaQsEu7DrcyWTeS80kzyTzcBb93820tVSzyeXcH4dzOQi9peRjRxvyKe98KBMl7AU6poKLqmtr8vLZfIROU7ol5dWESSpfoyPesLZhjB6juw3EwYZpCXrJVuPz8PuaY5uw9YfgDmYoA76G-NP6ajKDhVykyeaw38F2wcMcrd9ivZqAxtFMYTBulcAPOO9MkbazgxzigmNwBocR52j3OTg7mDfo1QgumdPH_wTdnH_9sbmorr5_u9x8uap0TdpcCdFDJ6GnctCsqfuuMUBE3_ZdbQQI4L3k1IwdNVA3cuSGtCNhnNOuUEA4P0GfH3z3c1-u0MbnCE7to50gLiqAVf9uvN2pbTgoIaRsOlYMPjwaxPBrNimrySZtnANvwpwUa7kglImmLej7_9DbMEdfzitUTYisuVwTnT1QOoaUohmfwlCi1mLVWqy6L7bA757Hf0L_1sj_ADvXoTw</recordid><startdate>20220101</startdate><enddate>20220101</enddate><creator>Pan, Xi-Chun</creator><creator>Xiong, Ya-Lan</creator><creator>Hong, Jia-Hui</creator><creator>Liu, Ya</creator><creator>Cen, Yan-Yan</creator><creator>Liu, Tao</creator><creator>Yang, Qun-Fang</creator><creator>Tao, Hui</creator><creator>Li, Yu-Nong</creator><creator>Zhang, Hai-Gang</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</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>8FI</scope><scope>8FJ</scope><scope>8FK</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>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20220101</creationdate><title>Cardiomyocytic FoxP3 is involved in Parkin-mediated mitophagy during cardiac remodeling and the regulatory role of triptolide</title><author>Pan, Xi-Chun ; Xiong, Ya-Lan ; Hong, Jia-Hui ; Liu, Ya ; Cen, Yan-Yan ; Liu, Tao ; Yang, Qun-Fang ; Tao, Hui ; Li, Yu-Nong ; Zhang, Hai-Gang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c406t-88ba79ab19dc254b75ea08b6b74e8a8a3b931ef71ea459f3e06f02331708ba033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Autophagy</topic><topic>Cardiomyocytes</topic><topic>Diterpenes</topic><topic>Epoxy Compounds</topic><topic>Forkhead Transcription Factors - metabolism</topic><topic>Heart</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>Mice</topic><topic>Mitochondria</topic><topic>Mitochondria - metabolism</topic><topic>Mitophagy - genetics</topic><topic>Phenanthrenes</topic><topic>Proteins</topic><topic>Reagents</topic><topic>Research Paper</topic><topic>RNA, Messenger - metabolism</topic><topic>Ubiquitin-Protein Ligases - metabolism</topic><topic>Ventricular Remodeling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pan, Xi-Chun</creatorcontrib><creatorcontrib>Xiong, Ya-Lan</creatorcontrib><creatorcontrib>Hong, Jia-Hui</creatorcontrib><creatorcontrib>Liu, Ya</creatorcontrib><creatorcontrib>Cen, Yan-Yan</creatorcontrib><creatorcontrib>Liu, Tao</creatorcontrib><creatorcontrib>Yang, Qun-Fang</creatorcontrib><creatorcontrib>Tao, Hui</creatorcontrib><creatorcontrib>Li, Yu-Nong</creatorcontrib><creatorcontrib>Zhang, Hai-Gang</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>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>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Theranostics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pan, Xi-Chun</au><au>Xiong, Ya-Lan</au><au>Hong, Jia-Hui</au><au>Liu, Ya</au><au>Cen, Yan-Yan</au><au>Liu, Tao</au><au>Yang, Qun-Fang</au><au>Tao, Hui</au><au>Li, Yu-Nong</au><au>Zhang, Hai-Gang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardiomyocytic FoxP3 is involved in Parkin-mediated mitophagy during cardiac remodeling and the regulatory role of triptolide</atitle><jtitle>Theranostics</jtitle><addtitle>Theranostics</addtitle><date>2022-01-01</date><risdate>2022</risdate><volume>12</volume><issue>5</issue><spage>2483</spage><epage>2501</epage><pages>2483-2501</pages><issn>1838-7640</issn><eissn>1838-7640</eissn><abstract>Forkhead/winged helix transcriptional factor P3 (FoxP3) is a well-studied transcription factor that maintains the activity of T cells, but whether cardiomyocytic FoxP3 participates in cardiac remodeling (CR) remains unclear. The present study was to investigate the role of cardiomyocytic FoxP3 in CR from the perspective of mitophagy.
CR was induced by angiotensin II (AngII)
, or by isoproterenol (Iso)
using male C57 mice or FoxP3
mice. Histological changes were observed by hematoxylin-eosin and Masson staining. Molecular changes were detected by immunohistochemistry, immunofluorescence, immunoblotting, and real-time PCR. Mitophagy was shaped by transmission electron microscopy and co-localization. The mRNA expression was operated by siRNA or adeno associated virus (AAV). Molecular interactions were detected by co-localization, immunoprecipitation (IP), and chromatin IP.
The expression and nuclear translocation of cardiomyocytic FoxP3 were downregulated in CR, while they were upregulated after triptolide (TP) treatment. In left ventricle (LV) remodeling in mice, autophagy was activated continuously in the myocardium, and TP significantly attenuated it. AngII induced massive mitophagy characterized by the activation of autophagy regulatory protein 5 (Atg5)-dependent autophagic flux. Critically, Parkin was identified as the main adaptor mediated myocardial mitophagy and was responsible for the effect of TP. Moreover, FoxP3 was responsible for the downregulation of Parkin and inhibited AngII-induced cardiac mitophagy. We found that mitophagy increased significantly and the inhibition of TP treatment reversed completely in FoxP3-deficient LVs. Mechanistically, FoxP3 interacted with a motif located downstream of the activating transcription 4 (ATF4)-binding motif involved in the promoter of
and hijacked free nuclear ATF4 to decrease
mRNA expression in CR.
Cardiomyocytic FoxP3 could negatively regulate Parkin-mediated mitophagy in CR, and restoring cardiomyocytic FoxP3 activity provided a cardioprotective strategy by inhibiting excessive cardiac mitophagy.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>35265221</pmid><doi>10.7150/thno.71102</doi><tpages>19</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access |
| subjects | Angiotensin II - pharmacology Animals Antibodies Autophagy Cardiomyocytes Diterpenes Epoxy Compounds Forkhead Transcription Factors - metabolism Heart Kinases Laboratory animals Male Mice Mitochondria Mitochondria - metabolism Mitophagy - genetics Phenanthrenes Proteins Reagents Research Paper RNA, Messenger - metabolism Ubiquitin-Protein Ligases - metabolism Ventricular Remodeling |
| title | Cardiomyocytic FoxP3 is involved in Parkin-mediated mitophagy during cardiac remodeling and the regulatory role of triptolide |
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