Qiliqiangxin inhibits angiotensin II‐induced transdifferentiation of rat cardiac fibroblasts through suppressing interleukin‐6
Qiliqiangxin (QL), a traditional Chinese medicine, had long been used to treat chronic heart failure. Recent studies revealed that differentiation of cardiac fibroblasts (CFs) into myofibroblasts played an important role in cardiac remodelling and development of heart failure, however, little was kn...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2015-05, Vol.19 (5), p.1114-1121 |
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| creator | Zhou, Jingmin Jiang, Kun Ding, Xuefeng Fu, Mingqiang Wang, Shijun Zhu, Lingti He, Tao Wang, Jingfeng Sun, Aijun Hu, Kai Chen, Li Zou, Yunzeng Ge, Junbo |
| description | Qiliqiangxin (QL), a traditional Chinese medicine, had long been used to treat chronic heart failure. Recent studies revealed that differentiation of cardiac fibroblasts (CFs) into myofibroblasts played an important role in cardiac remodelling and development of heart failure, however, little was known about the underlying mechanism and whether QL treatment being involved. This study aimed to investigate the effects of QL on angiotensin II (AngII)‐induced CFs transdifferentiation. Study was performed on in vitro cultured CFs from Sprague–Dawley rats. CFs differentiation was induced by AngII, which was attenuated by QL through reducing transforming growth factor‐β1 (TGF‐β1) and α‐smooth muscle actin (α‐SMA). Our data showed that AngII‐induced IL‐6 mRNA as well as typeI and typeIII collagens were reduced by QL. IL‐6 deficiency could suppress TGF‐β1 and α‐SMA, and both IL‐6 siRNA and QL‐mediated such effect was reversed by foresed expression of recombined IL‐6. Increase in actin stress fibres reflected the process of CFs differentiation, we found stress fibres were enhanced after AngII stimulation, which was attenuated by pre‐treating CFs with QL or IL‐6 siRNA, and re‐enhanced after rIL‐6 treatment. Importantly, we showed that calcineurin‐dependent NFAT3 nuclear translocation was essential to AngII‐mediated IL‐6 transcription, QL mimicked the effect of FK506, the calcineurin inhibitor, on suppression of IL‐6 expression and stress fibres formation. Collectively, our data demonstrated the negative regulation of CFs differentiation by QL through an IL‐6 transcriptional mechanism that depends on inhibition of calcineurin/NFAT3 signalling. |
| doi_str_mv | 10.1111/jcmm.12512 |
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| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4420613</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1677378400</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5142-71dec36f281e81a0960a49afc0d485659080a268b7e516894dc60a3a8955aa973</originalsourceid><addsrcrecordid>eNp9kc1u1DAURi0EomVgwwOgSGwQ0hTbsRN7g1SNWhjUCiHB2rpxnJk7JPbUTmi7QzwBz8iT1O0MFbDAG_8dHV_fj5DnjB6xPN5s7DAcMS4Zf0AOmVR8LnQpHu7XTJXqgDxJaUNpWbFSPyYHXNaSV0Iekh-fsMcLBL-6Ql-gX2ODYyryHsPofMqHy-Wv7z_Rt5N1bTFG8KnFrnPR-RFhxOCL0BURxsJCbBFs0WETQ9NDyqJxHcO0Whdp2m6jS9m3yq-MLvZu-oo-m6un5FEHfXLP9vOMfDk9-bx4Pz_7-G65OD6bW8kEn9esdbasOq6YUwyorigIDZ2lrVCykpoqCrxSTe0kq5QWrc1ECUpLCaDrckbe7rzbqRlca3P9EXqzjThAvDYB0Px943FtVuGbEYLT3LgseLUXxHAxuTSaAZN1fQ_ehSkZVtV1WSuR-zwjL_9BN2GKPn_PcK4prbnWLFOvd5SNIaXouvtiGDW30ZrbaM1dtBl-8Wf59-jvLDPAdsAl9u76PyrzYXF-vpPeAFcVs-k</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2290072991</pqid></control><display><type>article</type><title>Qiliqiangxin inhibits angiotensin II‐induced transdifferentiation of rat cardiac fibroblasts through suppressing interleukin‐6</title><source>MEDLINE</source><source>Wiley Journals</source><source>DOAJ Directory of Open Access Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Wiley Online Library (Open Access Collection)</source><source>PubMed Central</source><creator>Zhou, Jingmin ; Jiang, Kun ; Ding, Xuefeng ; Fu, Mingqiang ; Wang, Shijun ; Zhu, Lingti ; He, Tao ; Wang, Jingfeng ; Sun, Aijun ; Hu, Kai ; Chen, Li ; Zou, Yunzeng ; Ge, Junbo</creator><creatorcontrib>Zhou, Jingmin ; Jiang, Kun ; Ding, Xuefeng ; Fu, Mingqiang ; Wang, Shijun ; Zhu, Lingti ; He, Tao ; Wang, Jingfeng ; Sun, Aijun ; Hu, Kai ; Chen, Li ; Zou, Yunzeng ; Ge, Junbo</creatorcontrib><description>Qiliqiangxin (QL), a traditional Chinese medicine, had long been used to treat chronic heart failure. Recent studies revealed that differentiation of cardiac fibroblasts (CFs) into myofibroblasts played an important role in cardiac remodelling and development of heart failure, however, little was known about the underlying mechanism and whether QL treatment being involved. This study aimed to investigate the effects of QL on angiotensin II (AngII)‐induced CFs transdifferentiation. Study was performed on in vitro cultured CFs from Sprague–Dawley rats. CFs differentiation was induced by AngII, which was attenuated by QL through reducing transforming growth factor‐β1 (TGF‐β1) and α‐smooth muscle actin (α‐SMA). Our data showed that AngII‐induced IL‐6 mRNA as well as typeI and typeIII collagens were reduced by QL. IL‐6 deficiency could suppress TGF‐β1 and α‐SMA, and both IL‐6 siRNA and QL‐mediated such effect was reversed by foresed expression of recombined IL‐6. Increase in actin stress fibres reflected the process of CFs differentiation, we found stress fibres were enhanced after AngII stimulation, which was attenuated by pre‐treating CFs with QL or IL‐6 siRNA, and re‐enhanced after rIL‐6 treatment. Importantly, we showed that calcineurin‐dependent NFAT3 nuclear translocation was essential to AngII‐mediated IL‐6 transcription, QL mimicked the effect of FK506, the calcineurin inhibitor, on suppression of IL‐6 expression and stress fibres formation. Collectively, our data demonstrated the negative regulation of CFs differentiation by QL through an IL‐6 transcriptional mechanism that depends on inhibition of calcineurin/NFAT3 signalling.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.12512</identifier><identifier>PMID: 25752645</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Actin ; Actins - metabolism ; Angiotensin ; Angiotensin II ; Angiotensin II - pharmacology ; Animals ; Animals, Newborn ; Blotting, Western ; Calcineurin ; Calcineurin - metabolism ; Calcineurin inhibitors ; cardiac fibroblast ; Cardiac function ; Cardiomyopathy ; Cell Nucleus - drug effects ; Cell Nucleus - metabolism ; Cell Transdifferentiation - drug effects ; Collagen ; Congestive heart failure ; Cytokines ; Drugs, Chinese Herbal - pharmacology ; Fibroblasts ; Fibroblasts - drug effects ; Fibroblasts - metabolism ; Gene Expression - drug effects ; Heart ; Herbal medicine ; Inflammation ; Interleukin-6 - antagonists & inhibitors ; Interleukin-6 - genetics ; Interleukin-6 - metabolism ; interleukin‐6 ; Laboratory animals ; Microscopy, Fluorescence ; Muscles ; Myocardium - cytology ; NFAT3 ; NFATC Transcription Factors - metabolism ; Nuclear transport ; Original ; Polyclonal antibodies ; qiliqiangxin ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction ; RNA Interference ; Signal Transduction - drug effects ; siRNA ; Smooth muscle ; Stress ; Tacrolimus ; Traditional Chinese medicine ; Transcription ; transdifferentiation ; Transforming growth factor ; Transforming growth factor-b1 ; Translocation</subject><ispartof>Journal of cellular and molecular medicine, 2015-05, Vol.19 (5), p.1114-1121</ispartof><rights>2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2015. This work is published under http://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>2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5142-71dec36f281e81a0960a49afc0d485659080a268b7e516894dc60a3a8955aa973</citedby><cites>FETCH-LOGICAL-c5142-71dec36f281e81a0960a49afc0d485659080a268b7e516894dc60a3a8955aa973</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4420613/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4420613/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25752645$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Jingmin</creatorcontrib><creatorcontrib>Jiang, Kun</creatorcontrib><creatorcontrib>Ding, Xuefeng</creatorcontrib><creatorcontrib>Fu, Mingqiang</creatorcontrib><creatorcontrib>Wang, Shijun</creatorcontrib><creatorcontrib>Zhu, Lingti</creatorcontrib><creatorcontrib>He, Tao</creatorcontrib><creatorcontrib>Wang, Jingfeng</creatorcontrib><creatorcontrib>Sun, Aijun</creatorcontrib><creatorcontrib>Hu, Kai</creatorcontrib><creatorcontrib>Chen, Li</creatorcontrib><creatorcontrib>Zou, Yunzeng</creatorcontrib><creatorcontrib>Ge, Junbo</creatorcontrib><title>Qiliqiangxin inhibits angiotensin II‐induced transdifferentiation of rat cardiac fibroblasts through suppressing interleukin‐6</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Qiliqiangxin (QL), a traditional Chinese medicine, had long been used to treat chronic heart failure. Recent studies revealed that differentiation of cardiac fibroblasts (CFs) into myofibroblasts played an important role in cardiac remodelling and development of heart failure, however, little was known about the underlying mechanism and whether QL treatment being involved. This study aimed to investigate the effects of QL on angiotensin II (AngII)‐induced CFs transdifferentiation. Study was performed on in vitro cultured CFs from Sprague–Dawley rats. CFs differentiation was induced by AngII, which was attenuated by QL through reducing transforming growth factor‐β1 (TGF‐β1) and α‐smooth muscle actin (α‐SMA). Our data showed that AngII‐induced IL‐6 mRNA as well as typeI and typeIII collagens were reduced by QL. IL‐6 deficiency could suppress TGF‐β1 and α‐SMA, and both IL‐6 siRNA and QL‐mediated such effect was reversed by foresed expression of recombined IL‐6. Increase in actin stress fibres reflected the process of CFs differentiation, we found stress fibres were enhanced after AngII stimulation, which was attenuated by pre‐treating CFs with QL or IL‐6 siRNA, and re‐enhanced after rIL‐6 treatment. Importantly, we showed that calcineurin‐dependent NFAT3 nuclear translocation was essential to AngII‐mediated IL‐6 transcription, QL mimicked the effect of FK506, the calcineurin inhibitor, on suppression of IL‐6 expression and stress fibres formation. Collectively, our data demonstrated the negative regulation of CFs differentiation by QL through an IL‐6 transcriptional mechanism that depends on inhibition of calcineurin/NFAT3 signalling.</description><subject>Actin</subject><subject>Actins - metabolism</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Blotting, Western</subject><subject>Calcineurin</subject><subject>Calcineurin - metabolism</subject><subject>Calcineurin inhibitors</subject><subject>cardiac fibroblast</subject><subject>Cardiac function</subject><subject>Cardiomyopathy</subject><subject>Cell Nucleus - drug effects</subject><subject>Cell Nucleus - metabolism</subject><subject>Cell Transdifferentiation - drug effects</subject><subject>Collagen</subject><subject>Congestive heart failure</subject><subject>Cytokines</subject><subject>Drugs, Chinese Herbal - pharmacology</subject><subject>Fibroblasts</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - metabolism</subject><subject>Gene Expression - drug effects</subject><subject>Heart</subject><subject>Herbal medicine</subject><subject>Inflammation</subject><subject>Interleukin-6 - antagonists & inhibitors</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukin-6 - metabolism</subject><subject>interleukin‐6</subject><subject>Laboratory animals</subject><subject>Microscopy, Fluorescence</subject><subject>Muscles</subject><subject>Myocardium - cytology</subject><subject>NFAT3</subject><subject>NFATC Transcription Factors - metabolism</subject><subject>Nuclear transport</subject><subject>Original</subject><subject>Polyclonal antibodies</subject><subject>qiliqiangxin</subject><subject>Rats, Sprague-Dawley</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA Interference</subject><subject>Signal Transduction - drug effects</subject><subject>siRNA</subject><subject>Smooth muscle</subject><subject>Stress</subject><subject>Tacrolimus</subject><subject>Traditional Chinese medicine</subject><subject>Transcription</subject><subject>transdifferentiation</subject><subject>Transforming growth factor</subject><subject>Transforming growth factor-b1</subject><subject>Translocation</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><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>eNp9kc1u1DAURi0EomVgwwOgSGwQ0hTbsRN7g1SNWhjUCiHB2rpxnJk7JPbUTmi7QzwBz8iT1O0MFbDAG_8dHV_fj5DnjB6xPN5s7DAcMS4Zf0AOmVR8LnQpHu7XTJXqgDxJaUNpWbFSPyYHXNaSV0Iekh-fsMcLBL-6Ql-gX2ODYyryHsPofMqHy-Wv7z_Rt5N1bTFG8KnFrnPR-RFhxOCL0BURxsJCbBFs0WETQ9NDyqJxHcO0Whdp2m6jS9m3yq-MLvZu-oo-m6un5FEHfXLP9vOMfDk9-bx4Pz_7-G65OD6bW8kEn9esdbasOq6YUwyorigIDZ2lrVCykpoqCrxSTe0kq5QWrc1ECUpLCaDrckbe7rzbqRlca3P9EXqzjThAvDYB0Px943FtVuGbEYLT3LgseLUXxHAxuTSaAZN1fQ_ehSkZVtV1WSuR-zwjL_9BN2GKPn_PcK4prbnWLFOvd5SNIaXouvtiGDW30ZrbaM1dtBl-8Wf59-jvLDPAdsAl9u76PyrzYXF-vpPeAFcVs-k</recordid><startdate>201505</startdate><enddate>201505</enddate><creator>Zhou, Jingmin</creator><creator>Jiang, Kun</creator><creator>Ding, Xuefeng</creator><creator>Fu, Mingqiang</creator><creator>Wang, Shijun</creator><creator>Zhu, Lingti</creator><creator>He, Tao</creator><creator>Wang, Jingfeng</creator><creator>Sun, Aijun</creator><creator>Hu, Kai</creator><creator>Chen, Li</creator><creator>Zou, Yunzeng</creator><creator>Ge, Junbo</creator><general>John Wiley & Sons, Inc</general><general>BlackWell Publishing Ltd</general><scope>24P</scope><scope>WIN</scope><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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</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>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201505</creationdate><title>Qiliqiangxin inhibits angiotensin II‐induced transdifferentiation of rat cardiac fibroblasts through suppressing interleukin‐6</title><author>Zhou, Jingmin ; Jiang, Kun ; Ding, Xuefeng ; Fu, Mingqiang ; Wang, Shijun ; Zhu, Lingti ; He, Tao ; Wang, Jingfeng ; Sun, Aijun ; Hu, Kai ; Chen, Li ; Zou, Yunzeng ; Ge, Junbo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5142-71dec36f281e81a0960a49afc0d485659080a268b7e516894dc60a3a8955aa973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Actin</topic><topic>Actins - metabolism</topic><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Blotting, Western</topic><topic>Calcineurin</topic><topic>Calcineurin - metabolism</topic><topic>Calcineurin inhibitors</topic><topic>cardiac fibroblast</topic><topic>Cardiac function</topic><topic>Cardiomyopathy</topic><topic>Cell Nucleus - drug effects</topic><topic>Cell Nucleus - metabolism</topic><topic>Cell Transdifferentiation - drug effects</topic><topic>Collagen</topic><topic>Congestive heart failure</topic><topic>Cytokines</topic><topic>Drugs, Chinese Herbal - pharmacology</topic><topic>Fibroblasts</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - metabolism</topic><topic>Gene Expression - drug effects</topic><topic>Heart</topic><topic>Herbal medicine</topic><topic>Inflammation</topic><topic>Interleukin-6 - antagonists & inhibitors</topic><topic>Interleukin-6 - genetics</topic><topic>Interleukin-6 - metabolism</topic><topic>interleukin‐6</topic><topic>Laboratory animals</topic><topic>Microscopy, Fluorescence</topic><topic>Muscles</topic><topic>Myocardium - cytology</topic><topic>NFAT3</topic><topic>NFATC Transcription Factors - metabolism</topic><topic>Nuclear transport</topic><topic>Original</topic><topic>Polyclonal antibodies</topic><topic>qiliqiangxin</topic><topic>Rats, Sprague-Dawley</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA Interference</topic><topic>Signal Transduction - drug effects</topic><topic>siRNA</topic><topic>Smooth muscle</topic><topic>Stress</topic><topic>Tacrolimus</topic><topic>Traditional Chinese medicine</topic><topic>Transcription</topic><topic>transdifferentiation</topic><topic>Transforming growth factor</topic><topic>Transforming growth factor-b1</topic><topic>Translocation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Jingmin</creatorcontrib><creatorcontrib>Jiang, Kun</creatorcontrib><creatorcontrib>Ding, Xuefeng</creatorcontrib><creatorcontrib>Fu, Mingqiang</creatorcontrib><creatorcontrib>Wang, Shijun</creatorcontrib><creatorcontrib>Zhu, Lingti</creatorcontrib><creatorcontrib>He, Tao</creatorcontrib><creatorcontrib>Wang, Jingfeng</creatorcontrib><creatorcontrib>Sun, Aijun</creatorcontrib><creatorcontrib>Hu, Kai</creatorcontrib><creatorcontrib>Chen, Li</creatorcontrib><creatorcontrib>Zou, Yunzeng</creatorcontrib><creatorcontrib>Ge, Junbo</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Free Content</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences 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>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 Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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>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</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Jingmin</au><au>Jiang, Kun</au><au>Ding, Xuefeng</au><au>Fu, Mingqiang</au><au>Wang, Shijun</au><au>Zhu, Lingti</au><au>He, Tao</au><au>Wang, Jingfeng</au><au>Sun, Aijun</au><au>Hu, Kai</au><au>Chen, Li</au><au>Zou, Yunzeng</au><au>Ge, Junbo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Qiliqiangxin inhibits angiotensin II‐induced transdifferentiation of rat cardiac fibroblasts through suppressing interleukin‐6</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2015-05</date><risdate>2015</risdate><volume>19</volume><issue>5</issue><spage>1114</spage><epage>1121</epage><pages>1114-1121</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Qiliqiangxin (QL), a traditional Chinese medicine, had long been used to treat chronic heart failure. Recent studies revealed that differentiation of cardiac fibroblasts (CFs) into myofibroblasts played an important role in cardiac remodelling and development of heart failure, however, little was known about the underlying mechanism and whether QL treatment being involved. This study aimed to investigate the effects of QL on angiotensin II (AngII)‐induced CFs transdifferentiation. Study was performed on in vitro cultured CFs from Sprague–Dawley rats. CFs differentiation was induced by AngII, which was attenuated by QL through reducing transforming growth factor‐β1 (TGF‐β1) and α‐smooth muscle actin (α‐SMA). Our data showed that AngII‐induced IL‐6 mRNA as well as typeI and typeIII collagens were reduced by QL. IL‐6 deficiency could suppress TGF‐β1 and α‐SMA, and both IL‐6 siRNA and QL‐mediated such effect was reversed by foresed expression of recombined IL‐6. Increase in actin stress fibres reflected the process of CFs differentiation, we found stress fibres were enhanced after AngII stimulation, which was attenuated by pre‐treating CFs with QL or IL‐6 siRNA, and re‐enhanced after rIL‐6 treatment. Importantly, we showed that calcineurin‐dependent NFAT3 nuclear translocation was essential to AngII‐mediated IL‐6 transcription, QL mimicked the effect of FK506, the calcineurin inhibitor, on suppression of IL‐6 expression and stress fibres formation. Collectively, our data demonstrated the negative regulation of CFs differentiation by QL through an IL‐6 transcriptional mechanism that depends on inhibition of calcineurin/NFAT3 signalling.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>25752645</pmid><doi>10.1111/jcmm.12512</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of cellular and molecular medicine, 2015-05, Vol.19 (5), p.1114-1121 |
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| source | MEDLINE; Wiley Journals; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central |
| subjects | Actin Actins - metabolism Angiotensin Angiotensin II Angiotensin II - pharmacology Animals Animals, Newborn Blotting, Western Calcineurin Calcineurin - metabolism Calcineurin inhibitors cardiac fibroblast Cardiac function Cardiomyopathy Cell Nucleus - drug effects Cell Nucleus - metabolism Cell Transdifferentiation - drug effects Collagen Congestive heart failure Cytokines Drugs, Chinese Herbal - pharmacology Fibroblasts Fibroblasts - drug effects Fibroblasts - metabolism Gene Expression - drug effects Heart Herbal medicine Inflammation Interleukin-6 - antagonists & inhibitors Interleukin-6 - genetics Interleukin-6 - metabolism interleukin‐6 Laboratory animals Microscopy, Fluorescence Muscles Myocardium - cytology NFAT3 NFATC Transcription Factors - metabolism Nuclear transport Original Polyclonal antibodies qiliqiangxin Rats, Sprague-Dawley Reverse Transcriptase Polymerase Chain Reaction RNA Interference Signal Transduction - drug effects siRNA Smooth muscle Stress Tacrolimus Traditional Chinese medicine Transcription transdifferentiation Transforming growth factor Transforming growth factor-b1 Translocation |
| title | Qiliqiangxin inhibits angiotensin II‐induced transdifferentiation of rat cardiac fibroblasts through suppressing interleukin‐6 |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-04T08%3A33%3A40IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Qiliqiangxin%20inhibits%20angiotensin%20II%E2%80%90induced%20transdifferentiation%20of%20rat%20cardiac%20fibroblasts%20through%20suppressing%20interleukin%E2%80%906&rft.jtitle=Journal%20of%20cellular%20and%20molecular%20medicine&rft.au=Zhou,%20Jingmin&rft.date=2015-05&rft.volume=19&rft.issue=5&rft.spage=1114&rft.epage=1121&rft.pages=1114-1121&rft.issn=1582-1838&rft.eissn=1582-4934&rft_id=info:doi/10.1111/jcmm.12512&rft_dat=%3Cproquest_pubme%3E1677378400%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2290072991&rft_id=info:pmid/25752645&rfr_iscdi=true |