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Role of miR-128 in hypertension-induced myocardial injury
The present study aimed to investigate the role and mechanism of micro RNA (miR)-128 in hypertension-induced myocardial injury. The peripheral blood of patients with hypertension was collected and the expression of miR-128 was detected using fluorescence reverse transcription-quantitative polymerase...
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Published in: | Experimental and therapeutic medicine 2017-10, Vol.14 (4), p.2751-2756 |
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description | The present study aimed to investigate the role and mechanism of micro RNA (miR)-128 in hypertension-induced myocardial injury. The peripheral blood of patients with hypertension was collected and the expression of miR-128 was detected using fluorescence reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Primary myocardial cells isolated from rat
were cultured under conditions of hypoxia and glucose deprivation, and miR-128 expression was measured by RT-qPCR. The expression of c-Met protein was measured using western blot analysis and the apoptosis of transfected cells was measured by flow cytometry in rat myocardial cells following transfection with miR-128 mimics or c-Met siRNA. A luciferase assay was applied to assess the binding of miR-128 to c-Met mRNA. miR-128 expression was significantly higher in hypertension patients compared with controls (P |
doi_str_mv | 10.3892/etm.2017.4886 |
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were cultured under conditions of hypoxia and glucose deprivation, and miR-128 expression was measured by RT-qPCR. The expression of c-Met protein was measured using western blot analysis and the apoptosis of transfected cells was measured by flow cytometry in rat myocardial cells following transfection with miR-128 mimics or c-Met siRNA. A luciferase assay was applied to assess the binding of miR-128 to c-Met mRNA. miR-128 expression was significantly higher in hypertension patients compared with controls (P<0.05). miR-128 expression was higher in patients with stage III/IV hypertension compared with patients with stage II hypertension. Similarly, miR-128 expression in primary cardiomyocytes cultured under deprivation of oxygen and glucose increased with the culture time and reached a peak at 12 h. c-Met expression decreased significantly (P<0.05) and the ratio of apoptotic cells increased significantly (P<0.05), following transfection of miR-128 mimics. The number of apoptotic cells also increased when c-Met expression was knocked down by siRNA. The dual luciferase assay indicated that fluorescence intensity decreased significantly in miR-128 mimics and wild type c-Met group (P<0.05), indicating that miR-128 can directly target c-Met. Therefore, the results of the current study suggest that miR-128 may promote myocardial cell injury by regulating c-Met expression.</description><identifier>ISSN: 1792-0981</identifier><identifier>EISSN: 1792-1015</identifier><identifier>DOI: 10.3892/etm.2017.4886</identifier><identifier>PMID: 28928797</identifier><language>eng</language><publisher>Greece: Spandidos Publications UK Ltd</publisher><subject>Apoptosis ; Cardiomyocytes ; Glucose ; Heart attacks ; Heart failure ; Hypertension ; Phenols ; Proteins</subject><ispartof>Experimental and therapeutic medicine, 2017-10, Vol.14 (4), p.2751-2756</ispartof><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><rights>Copyright: © Yin et al. 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-3f33d12ae2817091485c01c6b2ee9893a53b67d75252149f801f31c11a22a4183</citedby><cites>FETCH-LOGICAL-c415t-3f33d12ae2817091485c01c6b2ee9893a53b67d75252149f801f31c11a22a4183</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/PMC5590046/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5590046/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28928797$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yin, Jie</creatorcontrib><creatorcontrib>Liu, Hongyan</creatorcontrib><creatorcontrib>Huan, Lei</creatorcontrib><creatorcontrib>Song, Suping</creatorcontrib><creatorcontrib>Han, Liying</creatorcontrib><creatorcontrib>Ren, Faxin</creatorcontrib><creatorcontrib>Zhang, Zengtang</creatorcontrib><creatorcontrib>Zang, Zhiqiang</creatorcontrib><creatorcontrib>Zhang, Junye</creatorcontrib><creatorcontrib>Wang, Shu</creatorcontrib><title>Role of miR-128 in hypertension-induced myocardial injury</title><title>Experimental and therapeutic medicine</title><addtitle>Exp Ther Med</addtitle><description>The present study aimed to investigate the role and mechanism of micro RNA (miR)-128 in hypertension-induced myocardial injury. The peripheral blood of patients with hypertension was collected and the expression of miR-128 was detected using fluorescence reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Primary myocardial cells isolated from rat
were cultured under conditions of hypoxia and glucose deprivation, and miR-128 expression was measured by RT-qPCR. The expression of c-Met protein was measured using western blot analysis and the apoptosis of transfected cells was measured by flow cytometry in rat myocardial cells following transfection with miR-128 mimics or c-Met siRNA. A luciferase assay was applied to assess the binding of miR-128 to c-Met mRNA. miR-128 expression was significantly higher in hypertension patients compared with controls (P<0.05). miR-128 expression was higher in patients with stage III/IV hypertension compared with patients with stage II hypertension. Similarly, miR-128 expression in primary cardiomyocytes cultured under deprivation of oxygen and glucose increased with the culture time and reached a peak at 12 h. c-Met expression decreased significantly (P<0.05) and the ratio of apoptotic cells increased significantly (P<0.05), following transfection of miR-128 mimics. The number of apoptotic cells also increased when c-Met expression was knocked down by siRNA. The dual luciferase assay indicated that fluorescence intensity decreased significantly in miR-128 mimics and wild type c-Met group (P<0.05), indicating that miR-128 can directly target c-Met. Therefore, the results of the current study suggest that miR-128 may promote myocardial cell injury by regulating c-Met expression.</description><subject>Apoptosis</subject><subject>Cardiomyocytes</subject><subject>Glucose</subject><subject>Heart attacks</subject><subject>Heart failure</subject><subject>Hypertension</subject><subject>Phenols</subject><subject>Proteins</subject><issn>1792-0981</issn><issn>1792-1015</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNpdkc9LwzAUx4MobswdvUrBi5fOvKRpk4sgw18wEIaeQ5amLqNtZtIK_e_N2BxqLgm8T7689z4IXQKeUS7IremaGcFQzDLO8xM0hkKQFDCw08MbCw4jNA1hg-NhOXDOztGIxM-8EMUYiaWrTeKqpLHLFAhPbJush63xnWmDdW1q27LXpkyawWnlS6vqiGx6P1ygs0rVwUwP9wS9Pz68zZ_TxevTy_x-keoMWJfSitISiDKEQ4EFZJxpDDpfEWMEF1QxusqLsmCEEchExTFUFDSAIkRlwOkE3e1zt_2qMaU2bedVLbfeNsoP0ikr_1Zau5Yf7ksyJjDO8hhwcwjw7rM3oZONDdrUtWqN64MEkUHcmWA4otf_0I3rfRvHi1QhACBnIlLpntLeheBNdWwGsNx5kdGL3HmROy-Rv_o9wZH-sUC_AWaBhqA</recordid><startdate>20171001</startdate><enddate>20171001</enddate><creator>Yin, Jie</creator><creator>Liu, Hongyan</creator><creator>Huan, Lei</creator><creator>Song, Suping</creator><creator>Han, Liying</creator><creator>Ren, Faxin</creator><creator>Zhang, Zengtang</creator><creator>Zang, Zhiqiang</creator><creator>Zhang, Junye</creator><creator>Wang, Shu</creator><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20171001</creationdate><title>Role of miR-128 in hypertension-induced myocardial injury</title><author>Yin, Jie ; Liu, Hongyan ; Huan, Lei ; Song, Suping ; Han, Liying ; Ren, Faxin ; Zhang, Zengtang ; Zang, Zhiqiang ; Zhang, Junye ; Wang, Shu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-3f33d12ae2817091485c01c6b2ee9893a53b67d75252149f801f31c11a22a4183</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Apoptosis</topic><topic>Cardiomyocytes</topic><topic>Glucose</topic><topic>Heart attacks</topic><topic>Heart failure</topic><topic>Hypertension</topic><topic>Phenols</topic><topic>Proteins</topic><toplevel>online_resources</toplevel><creatorcontrib>Yin, Jie</creatorcontrib><creatorcontrib>Liu, Hongyan</creatorcontrib><creatorcontrib>Huan, Lei</creatorcontrib><creatorcontrib>Song, Suping</creatorcontrib><creatorcontrib>Han, Liying</creatorcontrib><creatorcontrib>Ren, Faxin</creatorcontrib><creatorcontrib>Zhang, Zengtang</creatorcontrib><creatorcontrib>Zang, Zhiqiang</creatorcontrib><creatorcontrib>Zhang, Junye</creatorcontrib><creatorcontrib>Wang, Shu</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database (ProQuest)</collection><collection>ProQuest - Health & Medical Complete保健、医学与药学数据库</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)</collection><collection>ProQuest Central</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Nursing & Allied Health Premium</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>Experimental and therapeutic medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yin, Jie</au><au>Liu, Hongyan</au><au>Huan, Lei</au><au>Song, Suping</au><au>Han, Liying</au><au>Ren, Faxin</au><au>Zhang, Zengtang</au><au>Zang, Zhiqiang</au><au>Zhang, Junye</au><au>Wang, Shu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of miR-128 in hypertension-induced myocardial injury</atitle><jtitle>Experimental and therapeutic medicine</jtitle><addtitle>Exp Ther Med</addtitle><date>2017-10-01</date><risdate>2017</risdate><volume>14</volume><issue>4</issue><spage>2751</spage><epage>2756</epage><pages>2751-2756</pages><issn>1792-0981</issn><eissn>1792-1015</eissn><abstract>The present study aimed to investigate the role and mechanism of micro RNA (miR)-128 in hypertension-induced myocardial injury. The peripheral blood of patients with hypertension was collected and the expression of miR-128 was detected using fluorescence reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Primary myocardial cells isolated from rat
were cultured under conditions of hypoxia and glucose deprivation, and miR-128 expression was measured by RT-qPCR. The expression of c-Met protein was measured using western blot analysis and the apoptosis of transfected cells was measured by flow cytometry in rat myocardial cells following transfection with miR-128 mimics or c-Met siRNA. A luciferase assay was applied to assess the binding of miR-128 to c-Met mRNA. miR-128 expression was significantly higher in hypertension patients compared with controls (P<0.05). miR-128 expression was higher in patients with stage III/IV hypertension compared with patients with stage II hypertension. Similarly, miR-128 expression in primary cardiomyocytes cultured under deprivation of oxygen and glucose increased with the culture time and reached a peak at 12 h. c-Met expression decreased significantly (P<0.05) and the ratio of apoptotic cells increased significantly (P<0.05), following transfection of miR-128 mimics. The number of apoptotic cells also increased when c-Met expression was knocked down by siRNA. The dual luciferase assay indicated that fluorescence intensity decreased significantly in miR-128 mimics and wild type c-Met group (P<0.05), indicating that miR-128 can directly target c-Met. Therefore, the results of the current study suggest that miR-128 may promote myocardial cell injury by regulating c-Met expression.</abstract><cop>Greece</cop><pub>Spandidos Publications UK Ltd</pub><pmid>28928797</pmid><doi>10.3892/etm.2017.4886</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Apoptosis Cardiomyocytes Glucose Heart attacks Heart failure Hypertension Phenols Proteins |
title | Role of miR-128 in hypertension-induced myocardial injury |
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