Nucleolin promotes Ang II‑induced phenotypic transformation of vascular smooth muscle cells via interaction with tropoelastin mRNA
The current study aimed to clarify the role of nucleolin in the phenotypic transformation of vascular smooth muscle cells (VSMCs) and to preliminarily explore its underlying mechanism. The spatial and temporal expression patterns of nucleolin, and the effects of angiotensin II (Ang II) on the expres...
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| Veröffentlicht in: | International journal of molecular medicine 2019-04, Vol.43 (4), p.1597-1610 |
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| creator | Fang, Li Zhang, Peng-Fei Wang, Kang-Kai Xiao, Zhi-Lin Yang, Mei Yu, Zai-Xin |
| description | The current study aimed to clarify the role of nucleolin in the phenotypic transformation of vascular smooth muscle cells (VSMCs) and to preliminarily explore its underlying mechanism. The spatial and temporal expression patterns of nucleolin, and the effects of angiotensin II (Ang II) on the expression of VSMC phenotypic transformation markers, α‑smooth muscle‑actin, calponin, smooth muscle protein 22α and osteopontin were investigated. The effects of nucleolin on VSMC phenotypic transformation and the expression of phenotypic transformation‑associated genes, tropoelastin, epiregulin and fibroblast growth factor 2 (b‑FGF), were determined. Protein‑RNA co‑immunoprecipitation was used to investigate the potential target genes regulated by the nucleolin in phenotypic transformation of VSMCs. Finally, the stability of tropoelastin mRNA and the effects of nucleolin on the expression of tropoelastin were assayed. The results revealed that Ang II significantly promoted the phenotypic transformation of VSMCs. The expression of nucleolin was gradually upregulated in VSMCs treated with Ang II at different concentrations for various durations. Ang II induced nucleolin translocation from the nucleus to cytoplasm. Additionally, Ang II significantly promoted the phenotypic transformation of VSMCs. Overexpression and silencing of nucleolin regulated the expressions of tropoelastin, epiregulin and b‑FGF. There was an interaction between tropoelastin mRNA and nucleolin protein, promoting the stability of tropoelastin mRNA and enhancing the expression of tropoelastin at the protein level. Upregulation of nucleolin had an important role in Ang II‑induced VSMC phenotypic transformation, and its underlying mechanism may be through interacting with tropoelastin mRNA, leading to its increased stability and protein expression. The findings provide a new perspective into the regulatory mechanism of VSMC phenotypic transformation. |
| doi_str_mv | 10.3892/ijmm.2019.4090 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6414172</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A580345049</galeid><sourcerecordid>A580345049</sourcerecordid><originalsourceid>FETCH-LOGICAL-c485t-87764acb8bd8fa29b824420b89c39bf8c2f3dfb914b35923ac701bbfc12175113</originalsourceid><addsrcrecordid>eNptks2KFDEUhQtxcMbRrUsJuK42f9WVbIRm8KdhmAFRcBeSVNKdppKUSapldm58AN_AZ_FRfBLTM-OoMGSRkHz33HvIaZpnCC4I4_il23m_wBDxBYUcPmhOUM9Riyn99LCeEexb0nfL4-ZxzjsIcUc5e9QcE9hjCDt40ny7mPVo4ugCmFL0sZgMVmHz88d6_evrdxeGWZsBTFsTYrmanAYlyZBtTF4WFwOIFuxl1vMoE8g-xrIFfs5VEmgzjhnsnQQuFJOkvua_uEqUFKdoRplLbevfX6yeNEdWjtk8vd1Pm49vXn84e9eeX75dn63OW01ZV1rW90sqtWJqYFZirlg1iqFiXBOuLNPYksEqjqgiHcdE6h4ipaxGGPUdQuS0eXWjO83Km0GbUO2MYkrOy3QlonTi_5fgtmIT92JJEUU9rgIvbgVS_DybXMQuzinUmQVGHJIlR5z9pTZyNMIFG6uY9i5rseoYJLSDlFdqcQ9V12C80zEY6-r9fQU6xZyTsXeDIygOaRCHNIhDGsQhDbXg-b927_A_309-AzYRtV4</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2190369198</pqid></control><display><type>article</type><title>Nucleolin promotes Ang II‑induced phenotypic transformation of vascular smooth muscle cells via interaction with tropoelastin mRNA</title><source>Spandidos Publications Journals</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Fang, Li ; Zhang, Peng-Fei ; Wang, Kang-Kai ; Xiao, Zhi-Lin ; Yang, Mei ; Yu, Zai-Xin</creator><creatorcontrib>Fang, Li ; Zhang, Peng-Fei ; Wang, Kang-Kai ; Xiao, Zhi-Lin ; Yang, Mei ; Yu, Zai-Xin</creatorcontrib><description>The current study aimed to clarify the role of nucleolin in the phenotypic transformation of vascular smooth muscle cells (VSMCs) and to preliminarily explore its underlying mechanism. The spatial and temporal expression patterns of nucleolin, and the effects of angiotensin II (Ang II) on the expression of VSMC phenotypic transformation markers, α‑smooth muscle‑actin, calponin, smooth muscle protein 22α and osteopontin were investigated. The effects of nucleolin on VSMC phenotypic transformation and the expression of phenotypic transformation‑associated genes, tropoelastin, epiregulin and fibroblast growth factor 2 (b‑FGF), were determined. Protein‑RNA co‑immunoprecipitation was used to investigate the potential target genes regulated by the nucleolin in phenotypic transformation of VSMCs. Finally, the stability of tropoelastin mRNA and the effects of nucleolin on the expression of tropoelastin were assayed. The results revealed that Ang II significantly promoted the phenotypic transformation of VSMCs. The expression of nucleolin was gradually upregulated in VSMCs treated with Ang II at different concentrations for various durations. Ang II induced nucleolin translocation from the nucleus to cytoplasm. Additionally, Ang II significantly promoted the phenotypic transformation of VSMCs. Overexpression and silencing of nucleolin regulated the expressions of tropoelastin, epiregulin and b‑FGF. There was an interaction between tropoelastin mRNA and nucleolin protein, promoting the stability of tropoelastin mRNA and enhancing the expression of tropoelastin at the protein level. Upregulation of nucleolin had an important role in Ang II‑induced VSMC phenotypic transformation, and its underlying mechanism may be through interacting with tropoelastin mRNA, leading to its increased stability and protein expression. The findings provide a new perspective into the regulatory mechanism of VSMC phenotypic transformation.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.2019.4090</identifier><identifier>PMID: 30720050</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Actin ; Angiotensin II ; Angiotensins ; Animals ; Apoptosis ; Cardiovascular disease ; Cell growth ; Cell Line, Transformed ; Cytoplasm ; Epidermal growth factor ; Epiregulin - genetics ; Epiregulin - metabolism ; Fibroblast Growth Factor 2 - genetics ; Fibroblast Growth Factor 2 - metabolism ; Fibroblast growth factors ; Fibroblasts ; Gene expression ; Gene Silencing ; Genes ; Genetic aspects ; Genotype & phenotype ; Hypertension ; Kinases ; Localization ; Messenger RNA ; Muscle proteins ; Muscle, Smooth, Vascular - pathology ; Myocytes, Smooth Muscle - metabolism ; Nucleolin ; Phenotype ; Phosphoproteins - metabolism ; Physiological aspects ; Physiology ; Protein Binding ; Proteins ; Rats ; RNA ; RNA Stability - genetics ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; RNA-Binding Proteins - metabolism ; Smooth muscle ; Studies ; Tropoelastin - genetics ; Tropoelastin - metabolism ; Tumor necrosis factor-TNF</subject><ispartof>International journal of molecular medicine, 2019-04, Vol.43 (4), p.1597-1610</ispartof><rights>COPYRIGHT 2019 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><rights>Copyright: © Fang et al. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c485t-87764acb8bd8fa29b824420b89c39bf8c2f3dfb914b35923ac701bbfc12175113</citedby><cites>FETCH-LOGICAL-c485t-87764acb8bd8fa29b824420b89c39bf8c2f3dfb914b35923ac701bbfc12175113</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30720050$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fang, Li</creatorcontrib><creatorcontrib>Zhang, Peng-Fei</creatorcontrib><creatorcontrib>Wang, Kang-Kai</creatorcontrib><creatorcontrib>Xiao, Zhi-Lin</creatorcontrib><creatorcontrib>Yang, Mei</creatorcontrib><creatorcontrib>Yu, Zai-Xin</creatorcontrib><title>Nucleolin promotes Ang II‑induced phenotypic transformation of vascular smooth muscle cells via interaction with tropoelastin mRNA</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>The current study aimed to clarify the role of nucleolin in the phenotypic transformation of vascular smooth muscle cells (VSMCs) and to preliminarily explore its underlying mechanism. The spatial and temporal expression patterns of nucleolin, and the effects of angiotensin II (Ang II) on the expression of VSMC phenotypic transformation markers, α‑smooth muscle‑actin, calponin, smooth muscle protein 22α and osteopontin were investigated. The effects of nucleolin on VSMC phenotypic transformation and the expression of phenotypic transformation‑associated genes, tropoelastin, epiregulin and fibroblast growth factor 2 (b‑FGF), were determined. Protein‑RNA co‑immunoprecipitation was used to investigate the potential target genes regulated by the nucleolin in phenotypic transformation of VSMCs. Finally, the stability of tropoelastin mRNA and the effects of nucleolin on the expression of tropoelastin were assayed. The results revealed that Ang II significantly promoted the phenotypic transformation of VSMCs. The expression of nucleolin was gradually upregulated in VSMCs treated with Ang II at different concentrations for various durations. Ang II induced nucleolin translocation from the nucleus to cytoplasm. Additionally, Ang II significantly promoted the phenotypic transformation of VSMCs. Overexpression and silencing of nucleolin regulated the expressions of tropoelastin, epiregulin and b‑FGF. There was an interaction between tropoelastin mRNA and nucleolin protein, promoting the stability of tropoelastin mRNA and enhancing the expression of tropoelastin at the protein level. Upregulation of nucleolin had an important role in Ang II‑induced VSMC phenotypic transformation, and its underlying mechanism may be through interacting with tropoelastin mRNA, leading to its increased stability and protein expression. The findings provide a new perspective into the regulatory mechanism of VSMC phenotypic transformation.</description><subject>Actin</subject><subject>Angiotensin II</subject><subject>Angiotensins</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cardiovascular disease</subject><subject>Cell growth</subject><subject>Cell Line, Transformed</subject><subject>Cytoplasm</subject><subject>Epidermal growth factor</subject><subject>Epiregulin - genetics</subject><subject>Epiregulin - metabolism</subject><subject>Fibroblast Growth Factor 2 - genetics</subject><subject>Fibroblast Growth Factor 2 - metabolism</subject><subject>Fibroblast growth factors</subject><subject>Fibroblasts</subject><subject>Gene expression</subject><subject>Gene Silencing</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genotype & phenotype</subject><subject>Hypertension</subject><subject>Kinases</subject><subject>Localization</subject><subject>Messenger RNA</subject><subject>Muscle proteins</subject><subject>Muscle, Smooth, Vascular - pathology</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Nucleolin</subject><subject>Phenotype</subject><subject>Phosphoproteins - metabolism</subject><subject>Physiological aspects</subject><subject>Physiology</subject><subject>Protein Binding</subject><subject>Proteins</subject><subject>Rats</subject><subject>RNA</subject><subject>RNA Stability - genetics</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Smooth muscle</subject><subject>Studies</subject><subject>Tropoelastin - genetics</subject><subject>Tropoelastin - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptks2KFDEUhQtxcMbRrUsJuK42f9WVbIRm8KdhmAFRcBeSVNKdppKUSapldm58AN_AZ_FRfBLTM-OoMGSRkHz33HvIaZpnCC4I4_il23m_wBDxBYUcPmhOUM9Riyn99LCeEexb0nfL4-ZxzjsIcUc5e9QcE9hjCDt40ny7mPVo4ugCmFL0sZgMVmHz88d6_evrdxeGWZsBTFsTYrmanAYlyZBtTF4WFwOIFuxl1vMoE8g-xrIFfs5VEmgzjhnsnQQuFJOkvua_uEqUFKdoRplLbevfX6yeNEdWjtk8vd1Pm49vXn84e9eeX75dn63OW01ZV1rW90sqtWJqYFZirlg1iqFiXBOuLNPYksEqjqgiHcdE6h4ipaxGGPUdQuS0eXWjO83Km0GbUO2MYkrOy3QlonTi_5fgtmIT92JJEUU9rgIvbgVS_DybXMQuzinUmQVGHJIlR5z9pTZyNMIFG6uY9i5rseoYJLSDlFdqcQ9V12C80zEY6-r9fQU6xZyTsXeDIygOaRCHNIhDGsQhDbXg-b927_A_309-AzYRtV4</recordid><startdate>20190401</startdate><enddate>20190401</enddate><creator>Fang, Li</creator><creator>Zhang, Peng-Fei</creator><creator>Wang, Kang-Kai</creator><creator>Xiao, Zhi-Lin</creator><creator>Yang, Mei</creator><creator>Yu, Zai-Xin</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</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>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20190401</creationdate><title>Nucleolin promotes Ang II‑induced phenotypic transformation of vascular smooth muscle cells via interaction with tropoelastin mRNA</title><author>Fang, Li ; Zhang, Peng-Fei ; Wang, Kang-Kai ; Xiao, Zhi-Lin ; Yang, Mei ; Yu, Zai-Xin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c485t-87764acb8bd8fa29b824420b89c39bf8c2f3dfb914b35923ac701bbfc12175113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Actin</topic><topic>Angiotensin II</topic><topic>Angiotensins</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Cardiovascular disease</topic><topic>Cell growth</topic><topic>Cell Line, Transformed</topic><topic>Cytoplasm</topic><topic>Epidermal growth factor</topic><topic>Epiregulin - genetics</topic><topic>Epiregulin - metabolism</topic><topic>Fibroblast Growth Factor 2 - genetics</topic><topic>Fibroblast Growth Factor 2 - metabolism</topic><topic>Fibroblast growth factors</topic><topic>Fibroblasts</topic><topic>Gene expression</topic><topic>Gene Silencing</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genotype & phenotype</topic><topic>Hypertension</topic><topic>Kinases</topic><topic>Localization</topic><topic>Messenger RNA</topic><topic>Muscle proteins</topic><topic>Muscle, Smooth, Vascular - pathology</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>Nucleolin</topic><topic>Phenotype</topic><topic>Phosphoproteins - metabolism</topic><topic>Physiological aspects</topic><topic>Physiology</topic><topic>Protein Binding</topic><topic>Proteins</topic><topic>Rats</topic><topic>RNA</topic><topic>RNA Stability - genetics</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Smooth muscle</topic><topic>Studies</topic><topic>Tropoelastin - genetics</topic><topic>Tropoelastin - metabolism</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>online_resources</toplevel><creatorcontrib>Fang, Li</creatorcontrib><creatorcontrib>Zhang, Peng-Fei</creatorcontrib><creatorcontrib>Wang, Kang-Kai</creatorcontrib><creatorcontrib>Xiao, Zhi-Lin</creatorcontrib><creatorcontrib>Yang, Mei</creatorcontrib><creatorcontrib>Yu, Zai-Xin</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>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma 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</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>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fang, Li</au><au>Zhang, Peng-Fei</au><au>Wang, Kang-Kai</au><au>Xiao, Zhi-Lin</au><au>Yang, Mei</au><au>Yu, Zai-Xin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nucleolin promotes Ang II‑induced phenotypic transformation of vascular smooth muscle cells via interaction with tropoelastin mRNA</atitle><jtitle>International journal of molecular medicine</jtitle><addtitle>Int J Mol Med</addtitle><date>2019-04-01</date><risdate>2019</risdate><volume>43</volume><issue>4</issue><spage>1597</spage><epage>1610</epage><pages>1597-1610</pages><issn>1107-3756</issn><eissn>1791-244X</eissn><abstract>The current study aimed to clarify the role of nucleolin in the phenotypic transformation of vascular smooth muscle cells (VSMCs) and to preliminarily explore its underlying mechanism. The spatial and temporal expression patterns of nucleolin, and the effects of angiotensin II (Ang II) on the expression of VSMC phenotypic transformation markers, α‑smooth muscle‑actin, calponin, smooth muscle protein 22α and osteopontin were investigated. The effects of nucleolin on VSMC phenotypic transformation and the expression of phenotypic transformation‑associated genes, tropoelastin, epiregulin and fibroblast growth factor 2 (b‑FGF), were determined. Protein‑RNA co‑immunoprecipitation was used to investigate the potential target genes regulated by the nucleolin in phenotypic transformation of VSMCs. Finally, the stability of tropoelastin mRNA and the effects of nucleolin on the expression of tropoelastin were assayed. The results revealed that Ang II significantly promoted the phenotypic transformation of VSMCs. The expression of nucleolin was gradually upregulated in VSMCs treated with Ang II at different concentrations for various durations. Ang II induced nucleolin translocation from the nucleus to cytoplasm. Additionally, Ang II significantly promoted the phenotypic transformation of VSMCs. Overexpression and silencing of nucleolin regulated the expressions of tropoelastin, epiregulin and b‑FGF. There was an interaction between tropoelastin mRNA and nucleolin protein, promoting the stability of tropoelastin mRNA and enhancing the expression of tropoelastin at the protein level. Upregulation of nucleolin had an important role in Ang II‑induced VSMC phenotypic transformation, and its underlying mechanism may be through interacting with tropoelastin mRNA, leading to its increased stability and protein expression. The findings provide a new perspective into the regulatory mechanism of VSMC phenotypic transformation.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>30720050</pmid><doi>10.3892/ijmm.2019.4090</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Actin Angiotensin II Angiotensins Animals Apoptosis Cardiovascular disease Cell growth Cell Line, Transformed Cytoplasm Epidermal growth factor Epiregulin - genetics Epiregulin - metabolism Fibroblast Growth Factor 2 - genetics Fibroblast Growth Factor 2 - metabolism Fibroblast growth factors Fibroblasts Gene expression Gene Silencing Genes Genetic aspects Genotype & phenotype Hypertension Kinases Localization Messenger RNA Muscle proteins Muscle, Smooth, Vascular - pathology Myocytes, Smooth Muscle - metabolism Nucleolin Phenotype Phosphoproteins - metabolism Physiological aspects Physiology Protein Binding Proteins Rats RNA RNA Stability - genetics RNA, Messenger - genetics RNA, Messenger - metabolism RNA-Binding Proteins - metabolism Smooth muscle Studies Tropoelastin - genetics Tropoelastin - metabolism Tumor necrosis factor-TNF |
| title | Nucleolin promotes Ang II‑induced phenotypic transformation of vascular smooth muscle cells via interaction with tropoelastin mRNA |
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