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Expression of microRNA‐122 contributes to apoptosis in H9C2 myocytes
The microRNAs (miRNAs) can post‐transcriptionally regulate gene expression and heart development. The Pax‐8 gene knockout mice have apparent heart abnormalities. This study investigated the role of miRNAs in regulation of cardiac apoptosis and development in the knockout mice. MicroRNA microarrays d...
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Published in: | Journal of cellular and molecular medicine 2012-11, Vol.16 (11), p.2637-2646 |
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container_title | Journal of cellular and molecular medicine |
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creator | Huang, Xiaoyan Huang, Fang Yang, Deye Dong, Fengquan Shi, Xiangxiang Wang, Hongyu Zhou, Xi Wang, Suyun Dai, Shengchuan |
description | The microRNAs (miRNAs) can post‐transcriptionally regulate gene expression and heart development. The Pax‐8 gene knockout mice have apparent heart abnormalities. This study investigated the role of miRNAs in regulation of cardiac apoptosis and development in the knockout mice. MicroRNA microarrays demonstrated differential expression of microRNAs between Pax‐8−/− and Pax‐8+/− mice, confirmed by real‐time PCR. The miR‐122 was up‐regulated by 1.92 folds in Pax‐8−/− mice. There were ventricular septum defects in Pax‐8−/− mice, and increased numbers of apoptotic cells in the left ventricular wall and interventricular septum in Pax‐8−/− mice. In H9C2 myocytes, treatment with miR‐122 mimics or miR‐122 inhibitor affects the expression of CCK‐8 and activity of Caspase‐3. The miR‐122 is up‐regulated in the myocytes of Pax‐8−/− mice and may participate in the apoptotic gene expression and pathogenesis of heart development defect. |
doi_str_mv | 10.1111/j.1582-4934.2012.01577.x |
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The Pax‐8 gene knockout mice have apparent heart abnormalities. This study investigated the role of miRNAs in regulation of cardiac apoptosis and development in the knockout mice. MicroRNA microarrays demonstrated differential expression of microRNAs between Pax‐8−/− and Pax‐8+/− mice, confirmed by real‐time PCR. The miR‐122 was up‐regulated by 1.92 folds in Pax‐8−/− mice. There were ventricular septum defects in Pax‐8−/− mice, and increased numbers of apoptotic cells in the left ventricular wall and interventricular septum in Pax‐8−/− mice. In H9C2 myocytes, treatment with miR‐122 mimics or miR‐122 inhibitor affects the expression of CCK‐8 and activity of Caspase‐3. The miR‐122 is up‐regulated in the myocytes of Pax‐8−/− mice and may participate in the apoptotic gene expression and pathogenesis of heart development defect.</description><identifier>ISSN: 1582-1838</identifier><identifier>ISSN: 1582-4934</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/j.1582-4934.2012.01577.x</identifier><identifier>PMID: 22453009</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Animals ; apoptosis ; Apoptosis - genetics ; Caspase 3 - genetics ; Caspase 3 - metabolism ; Cells, Cultured ; differential expression ; Gene Expression Regulation, Developmental ; HAND2 ; Heart Septal Defects - genetics ; Heart Septal Defects - pathology ; Heart Septum - pathology ; Mice ; Mice, Knockout ; MicroRNAs - antagonists & inhibitors ; MicroRNAs - genetics ; miR‐122 ; Myocytes, Cardiac - pathology ; Myocytes, Cardiac - physiology ; Original ; Paired Box Transcription Factors - genetics ; PAX8 Transcription Factor ; RNA, Small Interfering ; Sincalide - genetics ; Sincalide - metabolism ; Transduction, Genetic ; Up-Regulation ; ventricular septum defect</subject><ispartof>Journal of cellular and molecular medicine, 2012-11, Vol.16 (11), p.2637-2646</ispartof><rights>2012 The Authors Journal of Cellular and Molecular Medicine © 2012 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd</rights><rights>2012 The Authors Journal of Cellular and Molecular Medicine © 2012 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.</rights><rights>2012. 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>2012 The Authors Journal of Cellular and Molecular Medicine © 2012 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2299178331/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2299178331?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,11541,25731,27901,27902,36989,36990,44566,46027,46451,53766,53768,74869</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1582-4934.2012.01577.x$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22453009$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Xiaoyan</creatorcontrib><creatorcontrib>Huang, Fang</creatorcontrib><creatorcontrib>Yang, Deye</creatorcontrib><creatorcontrib>Dong, Fengquan</creatorcontrib><creatorcontrib>Shi, Xiangxiang</creatorcontrib><creatorcontrib>Wang, Hongyu</creatorcontrib><creatorcontrib>Zhou, Xi</creatorcontrib><creatorcontrib>Wang, Suyun</creatorcontrib><creatorcontrib>Dai, Shengchuan</creatorcontrib><title>Expression of microRNA‐122 contributes to apoptosis in H9C2 myocytes</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>The microRNAs (miRNAs) can post‐transcriptionally regulate gene expression and heart development. The Pax‐8 gene knockout mice have apparent heart abnormalities. This study investigated the role of miRNAs in regulation of cardiac apoptosis and development in the knockout mice. MicroRNA microarrays demonstrated differential expression of microRNAs between Pax‐8−/− and Pax‐8+/− mice, confirmed by real‐time PCR. The miR‐122 was up‐regulated by 1.92 folds in Pax‐8−/− mice. There were ventricular septum defects in Pax‐8−/− mice, and increased numbers of apoptotic cells in the left ventricular wall and interventricular septum in Pax‐8−/− mice. In H9C2 myocytes, treatment with miR‐122 mimics or miR‐122 inhibitor affects the expression of CCK‐8 and activity of Caspase‐3. The miR‐122 is up‐regulated in the myocytes of Pax‐8−/− mice and may participate in the apoptotic gene expression and pathogenesis of heart development defect.</description><subject>Animals</subject><subject>apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Caspase 3 - genetics</subject><subject>Caspase 3 - metabolism</subject><subject>Cells, Cultured</subject><subject>differential expression</subject><subject>Gene Expression Regulation, Developmental</subject><subject>HAND2</subject><subject>Heart Septal Defects - genetics</subject><subject>Heart Septal Defects - pathology</subject><subject>Heart Septum - pathology</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>MicroRNAs - antagonists & inhibitors</subject><subject>MicroRNAs - genetics</subject><subject>miR‐122</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Myocytes, Cardiac - physiology</subject><subject>Original</subject><subject>Paired Box Transcription Factors - genetics</subject><subject>PAX8 Transcription Factor</subject><subject>RNA, Small Interfering</subject><subject>Sincalide - genetics</subject><subject>Sincalide - metabolism</subject><subject>Transduction, Genetic</subject><subject>Up-Regulation</subject><subject>ventricular septum defect</subject><issn>1582-1838</issn><issn>1582-4934</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNpdkc1u1DAUhS0EoqXwCsgSGzaT-l47cbJBqkb9AbUgoe4t_w04SuIQJzCz6yP0GfskJHQYfu7mXukcHR37I4QCy2Ce0zqDvMSVqLjIkAFmDHIps-0TcnwQnu5vKHl5RF6kVDPGC-DVc3KEKHLOWHVMLs63_eBTCrGjcUPbYIf4-ePZw909IFIbu3EIZhp9omOkuo_9GFNINHT0qlojbXfR7mb1JXm20U3yr_b7hNxenN-ur1bXny7fr8-uV7UocrlyvjQVsk3uBN-40nHNJDAmrUXpJELBjBGOO1EKqa00Go2RzhTG-so7zk_Iu8fYfjKtd9bP9XSj-iG0etipqIP6V-nCV_UlflcCoESOc8DbfcAQv00-jaoNyfqm0Z2PU1IAKGSeAxSz9c1_1jpOQze_TiFWFciSc5hdr_9udKjy-4f_VP4RGr876MDUQlLVaoGkFmBqIal-kVRb9WF9c7Oc_CfziJKd</recordid><startdate>201211</startdate><enddate>201211</enddate><creator>Huang, Xiaoyan</creator><creator>Huang, Fang</creator><creator>Yang, Deye</creator><creator>Dong, Fengquan</creator><creator>Shi, Xiangxiang</creator><creator>Wang, Hongyu</creator><creator>Zhou, Xi</creator><creator>Wang, Suyun</creator><creator>Dai, Shengchuan</creator><general>John Wiley & Sons, Inc</general><general>BlackWell Publishing Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</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>201211</creationdate><title>Expression of microRNA‐122 contributes to apoptosis in H9C2 myocytes</title><author>Huang, Xiaoyan ; Huang, Fang ; Yang, Deye ; Dong, Fengquan ; Shi, Xiangxiang ; Wang, Hongyu ; Zhou, Xi ; Wang, Suyun ; Dai, Shengchuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-j4657-de8b920f5d43fd8d3a071007cc27d72160bb4d3d4847ac7ba2bb7db6bce9ed33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Caspase 3 - genetics</topic><topic>Caspase 3 - metabolism</topic><topic>Cells, Cultured</topic><topic>differential expression</topic><topic>Gene Expression Regulation, Developmental</topic><topic>HAND2</topic><topic>Heart Septal Defects - genetics</topic><topic>Heart Septal Defects - pathology</topic><topic>Heart Septum - pathology</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>MicroRNAs - antagonists & inhibitors</topic><topic>MicroRNAs - genetics</topic><topic>miR‐122</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Myocytes, Cardiac - physiology</topic><topic>Original</topic><topic>Paired Box Transcription Factors - genetics</topic><topic>PAX8 Transcription Factor</topic><topic>RNA, Small Interfering</topic><topic>Sincalide - genetics</topic><topic>Sincalide - metabolism</topic><topic>Transduction, Genetic</topic><topic>Up-Regulation</topic><topic>ventricular septum defect</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Xiaoyan</creatorcontrib><creatorcontrib>Huang, Fang</creatorcontrib><creatorcontrib>Yang, Deye</creatorcontrib><creatorcontrib>Dong, Fengquan</creatorcontrib><creatorcontrib>Shi, Xiangxiang</creatorcontrib><creatorcontrib>Wang, Hongyu</creatorcontrib><creatorcontrib>Zhou, Xi</creatorcontrib><creatorcontrib>Wang, Suyun</creatorcontrib><creatorcontrib>Dai, Shengchuan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</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)</collection><collection>ProQuest Central</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</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>Biological Sciences</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_linktorsrc</fulltext></delivery><addata><au>Huang, Xiaoyan</au><au>Huang, Fang</au><au>Yang, Deye</au><au>Dong, Fengquan</au><au>Shi, Xiangxiang</au><au>Wang, Hongyu</au><au>Zhou, Xi</au><au>Wang, Suyun</au><au>Dai, Shengchuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of microRNA‐122 contributes to apoptosis in H9C2 myocytes</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2012-11</date><risdate>2012</risdate><volume>16</volume><issue>11</issue><spage>2637</spage><epage>2646</epage><pages>2637-2646</pages><issn>1582-1838</issn><issn>1582-4934</issn><eissn>1582-4934</eissn><abstract>The microRNAs (miRNAs) can post‐transcriptionally regulate gene expression and heart development. The Pax‐8 gene knockout mice have apparent heart abnormalities. This study investigated the role of miRNAs in regulation of cardiac apoptosis and development in the knockout mice. MicroRNA microarrays demonstrated differential expression of microRNAs between Pax‐8−/− and Pax‐8+/− mice, confirmed by real‐time PCR. The miR‐122 was up‐regulated by 1.92 folds in Pax‐8−/− mice. There were ventricular septum defects in Pax‐8−/− mice, and increased numbers of apoptotic cells in the left ventricular wall and interventricular septum in Pax‐8−/− mice. In H9C2 myocytes, treatment with miR‐122 mimics or miR‐122 inhibitor affects the expression of CCK‐8 and activity of Caspase‐3. The miR‐122 is up‐regulated in the myocytes of Pax‐8−/− mice and may participate in the apoptotic gene expression and pathogenesis of heart development defect.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>22453009</pmid><doi>10.1111/j.1582-4934.2012.01577.x</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals apoptosis Apoptosis - genetics Caspase 3 - genetics Caspase 3 - metabolism Cells, Cultured differential expression Gene Expression Regulation, Developmental HAND2 Heart Septal Defects - genetics Heart Septal Defects - pathology Heart Septum - pathology Mice Mice, Knockout MicroRNAs - antagonists & inhibitors MicroRNAs - genetics miR‐122 Myocytes, Cardiac - pathology Myocytes, Cardiac - physiology Original Paired Box Transcription Factors - genetics PAX8 Transcription Factor RNA, Small Interfering Sincalide - genetics Sincalide - metabolism Transduction, Genetic Up-Regulation ventricular septum defect |
title | Expression of microRNA‐122 contributes to apoptosis in H9C2 myocytes |
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