C/EBPβ knockdown protects cardiomyocytes from hypertrophy via inhibition of p65-NFκB
We investigated the role of C/EBPβ in mediating pathological cardiac hypertrophy. The results showed that the expression of C/EBPβ were significantly increased in response to hypertrophic stimulation in vitro and in vivo. C/EBPβ knockdown diminished the nuclear translocation and DNA binding activity...
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| Veröffentlicht in: | Molecular and cellular endocrinology 2014-06, Vol.390 (1-2), p.18-25 |
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| container_title | Molecular and cellular endocrinology |
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| creator | Zou, Jian Li, Hong Chen, Xi Zeng, Siyu Ye, Jiantao Zhou, Changhua Liu, Min Zhang, Luankun Yu, Na Gan, Xiaohong Zhou, Houfeng Xian, Zhiwei Chen, Shaorui Liu, Peiqing |
| description | We investigated the role of C/EBPβ in mediating pathological cardiac hypertrophy. The results showed that the expression of C/EBPβ were significantly increased in response to hypertrophic stimulation in vitro and in vivo. C/EBPβ knockdown diminished the nuclear translocation and DNA binding activity of p65-NFκB, and thereby inhibited cardiac hypertrophy. [Display omitted]
•C/EBPβ expression is upregulated in response to hypertrophic stimulation in vitro and in vivo.•C/EBPβ knockdown protects cardiomyocytes from hypertrophy.•C/EBPβ knockdown reduced the nuclear translocation of p65-NFκB, and diminished NFκB-DNA binding activity.
C/EBPβ, a member of the bHLH gene family of DNA-binding transcription factors, has been indicated as a central signal in physiologic hypertrophy. However, the role of C/EBPβ in pathological cardiac hypertrophy remains to be elucidated. In this study, we revealed that C/EBPβ is involved in cardiac hypertrophy, the expression of C/EBPβ were significantly increased in response to hypertrophic stimulation in vitro and in vivo. C/EBPβ knockdown inhibited PE-induced cardiac hypertrophy, and diminished the nuclear translocation and DNA binding activity of p65-NFκB. These results suggested that C/EBPβ knockdown protected cardiomyocytes from hypertrophy, which may be attributed to inhibition of NFκB-dependent transcriptional activity. These findings shed new light on the understanding of C/EBPβ-related cardiomyopathy, and suggest the potential application of C/EBPβ inhibitors in cardiac hypertrophy. |
| doi_str_mv | 10.1016/j.mce.2014.03.007 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1671572184</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0303720714000987</els_id><sourcerecordid>1671572184</sourcerecordid><originalsourceid>FETCH-LOGICAL-c419t-9d3fb164db65fd51febc6ea21618a9f402159318ba25b510c0ba3984b5bbcf673</originalsourceid><addsrcrecordid>eNqFkMFu1DAURS0EokPhA9ggL9kk9bNjOxErOmqhUkW7KGwt27E1nk7iYGeK8lss-Yh-U11NyxJWb3PuvU8HofdAaiAgTrb1YF1NCTQ1YTUh8gVaQStp1RIuX6IVYYRVkhJ5hN7kvCWF4LR9jY5oI0lDhVihH-uTs9Pr-9_4doz2to-_RjylODs7Z2x16kMclmiX2WXsUxzwZplcmlOcNgu-CxqHcRNMmEMccfR4Erz6dn7_5_QteuX1Lrt3T_cYfT8_u1l_rS6vvlysP19WtoFurrqeeQOi6Y3gvufgnbHCaQoCWt35hlDgHYPWaMoNB2KJ0axrG8ONsV5Idow-HnrL0z_3Ls9qCNm63U6PLu6zAiGBSwpt83-UlwHBWsYKCgfUpphzcl5NKQw6LQqIejSvtqqYV4_mFWGqeC2ZD0_1ezO4_m_iWXUBPh0AV3zcBZdUtsGN1vUhFd2qj-Ef9Q8KO5SU</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1551063833</pqid></control><display><type>article</type><title>C/EBPβ knockdown protects cardiomyocytes from hypertrophy via inhibition of p65-NFκB</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Zou, Jian ; Li, Hong ; Chen, Xi ; Zeng, Siyu ; Ye, Jiantao ; Zhou, Changhua ; Liu, Min ; Zhang, Luankun ; Yu, Na ; Gan, Xiaohong ; Zhou, Houfeng ; Xian, Zhiwei ; Chen, Shaorui ; Liu, Peiqing</creator><creatorcontrib>Zou, Jian ; Li, Hong ; Chen, Xi ; Zeng, Siyu ; Ye, Jiantao ; Zhou, Changhua ; Liu, Min ; Zhang, Luankun ; Yu, Na ; Gan, Xiaohong ; Zhou, Houfeng ; Xian, Zhiwei ; Chen, Shaorui ; Liu, Peiqing</creatorcontrib><description>We investigated the role of C/EBPβ in mediating pathological cardiac hypertrophy. The results showed that the expression of C/EBPβ were significantly increased in response to hypertrophic stimulation in vitro and in vivo. C/EBPβ knockdown diminished the nuclear translocation and DNA binding activity of p65-NFκB, and thereby inhibited cardiac hypertrophy. [Display omitted]
•C/EBPβ expression is upregulated in response to hypertrophic stimulation in vitro and in vivo.•C/EBPβ knockdown protects cardiomyocytes from hypertrophy.•C/EBPβ knockdown reduced the nuclear translocation of p65-NFκB, and diminished NFκB-DNA binding activity.
C/EBPβ, a member of the bHLH gene family of DNA-binding transcription factors, has been indicated as a central signal in physiologic hypertrophy. However, the role of C/EBPβ in pathological cardiac hypertrophy remains to be elucidated. In this study, we revealed that C/EBPβ is involved in cardiac hypertrophy, the expression of C/EBPβ were significantly increased in response to hypertrophic stimulation in vitro and in vivo. C/EBPβ knockdown inhibited PE-induced cardiac hypertrophy, and diminished the nuclear translocation and DNA binding activity of p65-NFκB. These results suggested that C/EBPβ knockdown protected cardiomyocytes from hypertrophy, which may be attributed to inhibition of NFκB-dependent transcriptional activity. These findings shed new light on the understanding of C/EBPβ-related cardiomyopathy, and suggest the potential application of C/EBPβ inhibitors in cardiac hypertrophy.</description><identifier>ISSN: 0303-7207</identifier><identifier>EISSN: 1872-8057</identifier><identifier>DOI: 10.1016/j.mce.2014.03.007</identifier><identifier>PMID: 24704266</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Active Transport, Cell Nucleus ; Animals ; Binding ; Biomedical materials ; C/EBPβ ; Cardiac hypertrophy ; CCAAT-Enhancer-Binding Protein-beta - genetics ; CCAAT-Enhancer-Binding Protein-beta - metabolism ; Cells, Cultured ; DNA - metabolism ; Electrophoretic Mobility Shift Assay ; Gene Expression ; Gene Knockdown Techniques ; Genes ; Hypertrophy - metabolism ; In vivo testing ; In vivo tests ; Inhibition ; Inhibitors ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; p65-NFκB ; Protein Binding ; Rats, Sprague-Dawley ; Stimulation ; Transcription Factor RelA - genetics ; Transcription Factor RelA - metabolism</subject><ispartof>Molecular and cellular endocrinology, 2014-06, Vol.390 (1-2), p.18-25</ispartof><rights>2014 Elsevier Ireland Ltd</rights><rights>Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-9d3fb164db65fd51febc6ea21618a9f402159318ba25b510c0ba3984b5bbcf673</citedby><cites>FETCH-LOGICAL-c419t-9d3fb164db65fd51febc6ea21618a9f402159318ba25b510c0ba3984b5bbcf673</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0303720714000987$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24704266$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zou, Jian</creatorcontrib><creatorcontrib>Li, Hong</creatorcontrib><creatorcontrib>Chen, Xi</creatorcontrib><creatorcontrib>Zeng, Siyu</creatorcontrib><creatorcontrib>Ye, Jiantao</creatorcontrib><creatorcontrib>Zhou, Changhua</creatorcontrib><creatorcontrib>Liu, Min</creatorcontrib><creatorcontrib>Zhang, Luankun</creatorcontrib><creatorcontrib>Yu, Na</creatorcontrib><creatorcontrib>Gan, Xiaohong</creatorcontrib><creatorcontrib>Zhou, Houfeng</creatorcontrib><creatorcontrib>Xian, Zhiwei</creatorcontrib><creatorcontrib>Chen, Shaorui</creatorcontrib><creatorcontrib>Liu, Peiqing</creatorcontrib><title>C/EBPβ knockdown protects cardiomyocytes from hypertrophy via inhibition of p65-NFκB</title><title>Molecular and cellular endocrinology</title><addtitle>Mol Cell Endocrinol</addtitle><description>We investigated the role of C/EBPβ in mediating pathological cardiac hypertrophy. The results showed that the expression of C/EBPβ were significantly increased in response to hypertrophic stimulation in vitro and in vivo. C/EBPβ knockdown diminished the nuclear translocation and DNA binding activity of p65-NFκB, and thereby inhibited cardiac hypertrophy. [Display omitted]
•C/EBPβ expression is upregulated in response to hypertrophic stimulation in vitro and in vivo.•C/EBPβ knockdown protects cardiomyocytes from hypertrophy.•C/EBPβ knockdown reduced the nuclear translocation of p65-NFκB, and diminished NFκB-DNA binding activity.
C/EBPβ, a member of the bHLH gene family of DNA-binding transcription factors, has been indicated as a central signal in physiologic hypertrophy. However, the role of C/EBPβ in pathological cardiac hypertrophy remains to be elucidated. In this study, we revealed that C/EBPβ is involved in cardiac hypertrophy, the expression of C/EBPβ were significantly increased in response to hypertrophic stimulation in vitro and in vivo. C/EBPβ knockdown inhibited PE-induced cardiac hypertrophy, and diminished the nuclear translocation and DNA binding activity of p65-NFκB. These results suggested that C/EBPβ knockdown protected cardiomyocytes from hypertrophy, which may be attributed to inhibition of NFκB-dependent transcriptional activity. These findings shed new light on the understanding of C/EBPβ-related cardiomyopathy, and suggest the potential application of C/EBPβ inhibitors in cardiac hypertrophy.</description><subject>Active Transport, Cell Nucleus</subject><subject>Animals</subject><subject>Binding</subject><subject>Biomedical materials</subject><subject>C/EBPβ</subject><subject>Cardiac hypertrophy</subject><subject>CCAAT-Enhancer-Binding Protein-beta - genetics</subject><subject>CCAAT-Enhancer-Binding Protein-beta - metabolism</subject><subject>Cells, Cultured</subject><subject>DNA - metabolism</subject><subject>Electrophoretic Mobility Shift Assay</subject><subject>Gene Expression</subject><subject>Gene Knockdown Techniques</subject><subject>Genes</subject><subject>Hypertrophy - metabolism</subject><subject>In vivo testing</subject><subject>In vivo tests</subject><subject>Inhibition</subject><subject>Inhibitors</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>p65-NFκB</subject><subject>Protein Binding</subject><subject>Rats, Sprague-Dawley</subject><subject>Stimulation</subject><subject>Transcription Factor RelA - genetics</subject><subject>Transcription Factor RelA - metabolism</subject><issn>0303-7207</issn><issn>1872-8057</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMFu1DAURS0EokPhA9ggL9kk9bNjOxErOmqhUkW7KGwt27E1nk7iYGeK8lss-Yh-U11NyxJWb3PuvU8HofdAaiAgTrb1YF1NCTQ1YTUh8gVaQStp1RIuX6IVYYRVkhJ5hN7kvCWF4LR9jY5oI0lDhVihH-uTs9Pr-9_4doz2to-_RjylODs7Z2x16kMclmiX2WXsUxzwZplcmlOcNgu-CxqHcRNMmEMccfR4Erz6dn7_5_QteuX1Lrt3T_cYfT8_u1l_rS6vvlysP19WtoFurrqeeQOi6Y3gvufgnbHCaQoCWt35hlDgHYPWaMoNB2KJ0axrG8ONsV5Idow-HnrL0z_3Ls9qCNm63U6PLu6zAiGBSwpt83-UlwHBWsYKCgfUpphzcl5NKQw6LQqIejSvtqqYV4_mFWGqeC2ZD0_1ezO4_m_iWXUBPh0AV3zcBZdUtsGN1vUhFd2qj-Ef9Q8KO5SU</recordid><startdate>20140605</startdate><enddate>20140605</enddate><creator>Zou, Jian</creator><creator>Li, Hong</creator><creator>Chen, Xi</creator><creator>Zeng, Siyu</creator><creator>Ye, Jiantao</creator><creator>Zhou, Changhua</creator><creator>Liu, Min</creator><creator>Zhang, Luankun</creator><creator>Yu, Na</creator><creator>Gan, Xiaohong</creator><creator>Zhou, Houfeng</creator><creator>Xian, Zhiwei</creator><creator>Chen, Shaorui</creator><creator>Liu, Peiqing</creator><general>Elsevier Ireland Ltd</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>7U5</scope><scope>8FD</scope><scope>L7M</scope></search><sort><creationdate>20140605</creationdate><title>C/EBPβ knockdown protects cardiomyocytes from hypertrophy via inhibition of p65-NFκB</title><author>Zou, Jian ; Li, Hong ; Chen, Xi ; Zeng, Siyu ; Ye, Jiantao ; Zhou, Changhua ; Liu, Min ; Zhang, Luankun ; Yu, Na ; Gan, Xiaohong ; Zhou, Houfeng ; Xian, Zhiwei ; Chen, Shaorui ; Liu, Peiqing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-9d3fb164db65fd51febc6ea21618a9f402159318ba25b510c0ba3984b5bbcf673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Active Transport, Cell Nucleus</topic><topic>Animals</topic><topic>Binding</topic><topic>Biomedical materials</topic><topic>C/EBPβ</topic><topic>Cardiac hypertrophy</topic><topic>CCAAT-Enhancer-Binding Protein-beta - genetics</topic><topic>CCAAT-Enhancer-Binding Protein-beta - metabolism</topic><topic>Cells, Cultured</topic><topic>DNA - metabolism</topic><topic>Electrophoretic Mobility Shift Assay</topic><topic>Gene Expression</topic><topic>Gene Knockdown Techniques</topic><topic>Genes</topic><topic>Hypertrophy - metabolism</topic><topic>In vivo testing</topic><topic>In vivo tests</topic><topic>Inhibition</topic><topic>Inhibitors</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - pathology</topic><topic>p65-NFκB</topic><topic>Protein Binding</topic><topic>Rats, Sprague-Dawley</topic><topic>Stimulation</topic><topic>Transcription Factor RelA - genetics</topic><topic>Transcription Factor RelA - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zou, Jian</creatorcontrib><creatorcontrib>Li, Hong</creatorcontrib><creatorcontrib>Chen, Xi</creatorcontrib><creatorcontrib>Zeng, Siyu</creatorcontrib><creatorcontrib>Ye, Jiantao</creatorcontrib><creatorcontrib>Zhou, Changhua</creatorcontrib><creatorcontrib>Liu, Min</creatorcontrib><creatorcontrib>Zhang, Luankun</creatorcontrib><creatorcontrib>Yu, Na</creatorcontrib><creatorcontrib>Gan, Xiaohong</creatorcontrib><creatorcontrib>Zhou, Houfeng</creatorcontrib><creatorcontrib>Xian, Zhiwei</creatorcontrib><creatorcontrib>Chen, Shaorui</creatorcontrib><creatorcontrib>Liu, Peiqing</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>Technology Research Database</collection><collection>Advanced Technologies Database with Aerospace</collection><jtitle>Molecular and cellular endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zou, Jian</au><au>Li, Hong</au><au>Chen, Xi</au><au>Zeng, Siyu</au><au>Ye, Jiantao</au><au>Zhou, Changhua</au><au>Liu, Min</au><au>Zhang, Luankun</au><au>Yu, Na</au><au>Gan, Xiaohong</au><au>Zhou, Houfeng</au><au>Xian, Zhiwei</au><au>Chen, Shaorui</au><au>Liu, Peiqing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>C/EBPβ knockdown protects cardiomyocytes from hypertrophy via inhibition of p65-NFκB</atitle><jtitle>Molecular and cellular endocrinology</jtitle><addtitle>Mol Cell Endocrinol</addtitle><date>2014-06-05</date><risdate>2014</risdate><volume>390</volume><issue>1-2</issue><spage>18</spage><epage>25</epage><pages>18-25</pages><issn>0303-7207</issn><eissn>1872-8057</eissn><abstract>We investigated the role of C/EBPβ in mediating pathological cardiac hypertrophy. The results showed that the expression of C/EBPβ were significantly increased in response to hypertrophic stimulation in vitro and in vivo. C/EBPβ knockdown diminished the nuclear translocation and DNA binding activity of p65-NFκB, and thereby inhibited cardiac hypertrophy. [Display omitted]
•C/EBPβ expression is upregulated in response to hypertrophic stimulation in vitro and in vivo.•C/EBPβ knockdown protects cardiomyocytes from hypertrophy.•C/EBPβ knockdown reduced the nuclear translocation of p65-NFκB, and diminished NFκB-DNA binding activity.
C/EBPβ, a member of the bHLH gene family of DNA-binding transcription factors, has been indicated as a central signal in physiologic hypertrophy. However, the role of C/EBPβ in pathological cardiac hypertrophy remains to be elucidated. In this study, we revealed that C/EBPβ is involved in cardiac hypertrophy, the expression of C/EBPβ were significantly increased in response to hypertrophic stimulation in vitro and in vivo. C/EBPβ knockdown inhibited PE-induced cardiac hypertrophy, and diminished the nuclear translocation and DNA binding activity of p65-NFκB. These results suggested that C/EBPβ knockdown protected cardiomyocytes from hypertrophy, which may be attributed to inhibition of NFκB-dependent transcriptional activity. These findings shed new light on the understanding of C/EBPβ-related cardiomyopathy, and suggest the potential application of C/EBPβ inhibitors in cardiac hypertrophy.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>24704266</pmid><doi>10.1016/j.mce.2014.03.007</doi><tpages>8</tpages></addata></record> |
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| ispartof | Molecular and cellular endocrinology, 2014-06, Vol.390 (1-2), p.18-25 |
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| subjects | Active Transport, Cell Nucleus Animals Binding Biomedical materials C/EBPβ Cardiac hypertrophy CCAAT-Enhancer-Binding Protein-beta - genetics CCAAT-Enhancer-Binding Protein-beta - metabolism Cells, Cultured DNA - metabolism Electrophoretic Mobility Shift Assay Gene Expression Gene Knockdown Techniques Genes Hypertrophy - metabolism In vivo testing In vivo tests Inhibition Inhibitors Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology p65-NFκB Protein Binding Rats, Sprague-Dawley Stimulation Transcription Factor RelA - genetics Transcription Factor RelA - metabolism |
| title | C/EBPβ knockdown protects cardiomyocytes from hypertrophy via inhibition of p65-NFκB |
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