Involvement of miR‐145 in the development of aortic dissection via inducing proliferation, migration, and apoptosis of vascular smooth muscle cells
Aim The current study aimed to examine miR‐145's contribution to thoracic aortic dissection (AD) development by modulating the biological functions of vascular smooth muscle cells (VSMCs). Methods The concentration of circulating miR‐145 was determined in patients with AD and healthy controls u...
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| Veröffentlicht in: | Journal of clinical laboratory analysis 2020-01, Vol.34 (1), p.e23028-n/a |
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| creator | Huang, Wenhui Huang, Cheng Ding, Huanyu Luo, Jianfang Liu, Yuan Fan, Ruixin Xiao, Fei Fan, Xiaoping Jiang, Zhisheng |
| description | Aim
The current study aimed to examine miR‐145's contribution to thoracic aortic dissection (AD) development by modulating the biological functions of vascular smooth muscle cells (VSMCs).
Methods
The concentration of circulating miR‐145 was determined in patients with AD and healthy controls using quantitative polymerase chain reaction (qPCR). Aortic specimens were obtained from both individuals with Stanford type A AD undergoing surgical treatment and deceased organ donors (serving as controls) whose causes of death were nonvascular diseases. Then, qPCR and fluorescence in situ hybridization were applied to assess miR‐145 amounts and location, respectively. Furthermore, qPCR and immunoblot were employed to determine SMAD3 (the target gene of miR‐145, involved in the TGF‐β pathway) amounts at the gene and protein levels, respectively. Moreover, in vitro transfection of VSMCs with miR‐145 mimics or inhibitors was conducted. Finally, the 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay, Transwell assay and flow cytometry were employed for detecting VSMC proliferation, migration, and apoptosis, respectively.
Results
The amounts of miR‐145 in plasma and aortic specimens were markedly reduced in the AD group in comparison with control values (P |
| doi_str_mv | 10.1002/jcla.23028 |
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The current study aimed to examine miR‐145's contribution to thoracic aortic dissection (AD) development by modulating the biological functions of vascular smooth muscle cells (VSMCs).
Methods
The concentration of circulating miR‐145 was determined in patients with AD and healthy controls using quantitative polymerase chain reaction (qPCR). Aortic specimens were obtained from both individuals with Stanford type A AD undergoing surgical treatment and deceased organ donors (serving as controls) whose causes of death were nonvascular diseases. Then, qPCR and fluorescence in situ hybridization were applied to assess miR‐145 amounts and location, respectively. Furthermore, qPCR and immunoblot were employed to determine SMAD3 (the target gene of miR‐145, involved in the TGF‐β pathway) amounts at the gene and protein levels, respectively. Moreover, in vitro transfection of VSMCs with miR‐145 mimics or inhibitors was conducted. Finally, the 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay, Transwell assay and flow cytometry were employed for detecting VSMC proliferation, migration, and apoptosis, respectively.
Results
The amounts of miR‐145 in plasma and aortic specimens were markedly reduced in the AD group in comparison with control values (P < .05). miR‐145 was mostly located in VSMCs. Proliferation and apoptosis of VSMCs were significantly induced in vitro by the downregulation of miR‐145. Also, miR‐145 modulated SMAD3 expression.
Conclusions
miR‐145 was found to be downregulated in patients with AD, which induced the proliferation, migration, and apoptosis of VSMCs by targeting SMAD3. This suggested the involvement of miR‐145 in the pathogenesis of AD.</description><identifier>ISSN: 0887-8013</identifier><identifier>EISSN: 1098-2825</identifier><identifier>DOI: 10.1002/jcla.23028</identifier><identifier>PMID: 31489719</identifier><language>eng</language><publisher>United States: John Wiley and Sons Inc</publisher><subject>Aged ; Aneurysm, Dissecting - genetics ; aortic dissection ; Apoptosis - genetics ; Base Sequence ; Cell Movement - genetics ; Cell Proliferation - genetics ; Female ; Gene Expression Regulation ; Humans ; Male ; MicroRNAs - blood ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Middle Aged ; miR‐145 ; Muscle, Smooth, Vascular - pathology ; Myocytes, Smooth Muscle - metabolism ; Myocytes, Smooth Muscle - pathology ; proliferation ; SMAD3 ; Smad3 Protein - metabolism ; vascular smooth muscle cell</subject><ispartof>Journal of clinical laboratory analysis, 2020-01, Vol.34 (1), p.e23028-n/a</ispartof><rights>2019 The Authors. published by Wiley Periodicals, Inc.</rights><rights>2019 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4868-e8aa9811f699511353d19af2b343a1cb22e63bd4c21d02eefba8215e464252fa3</citedby><cites>FETCH-LOGICAL-c4868-e8aa9811f699511353d19af2b343a1cb22e63bd4c21d02eefba8215e464252fa3</cites><orcidid>0000-0002-0307-9119 ; 0000-0003-3220-1280 ; 0000-0002-0702-588X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6977357/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6977357/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31489719$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Wenhui</creatorcontrib><creatorcontrib>Huang, Cheng</creatorcontrib><creatorcontrib>Ding, Huanyu</creatorcontrib><creatorcontrib>Luo, Jianfang</creatorcontrib><creatorcontrib>Liu, Yuan</creatorcontrib><creatorcontrib>Fan, Ruixin</creatorcontrib><creatorcontrib>Xiao, Fei</creatorcontrib><creatorcontrib>Fan, Xiaoping</creatorcontrib><creatorcontrib>Jiang, Zhisheng</creatorcontrib><title>Involvement of miR‐145 in the development of aortic dissection via inducing proliferation, migration, and apoptosis of vascular smooth muscle cells</title><title>Journal of clinical laboratory analysis</title><addtitle>J Clin Lab Anal</addtitle><description>Aim
The current study aimed to examine miR‐145's contribution to thoracic aortic dissection (AD) development by modulating the biological functions of vascular smooth muscle cells (VSMCs).
Methods
The concentration of circulating miR‐145 was determined in patients with AD and healthy controls using quantitative polymerase chain reaction (qPCR). Aortic specimens were obtained from both individuals with Stanford type A AD undergoing surgical treatment and deceased organ donors (serving as controls) whose causes of death were nonvascular diseases. Then, qPCR and fluorescence in situ hybridization were applied to assess miR‐145 amounts and location, respectively. Furthermore, qPCR and immunoblot were employed to determine SMAD3 (the target gene of miR‐145, involved in the TGF‐β pathway) amounts at the gene and protein levels, respectively. Moreover, in vitro transfection of VSMCs with miR‐145 mimics or inhibitors was conducted. Finally, the 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay, Transwell assay and flow cytometry were employed for detecting VSMC proliferation, migration, and apoptosis, respectively.
Results
The amounts of miR‐145 in plasma and aortic specimens were markedly reduced in the AD group in comparison with control values (P < .05). miR‐145 was mostly located in VSMCs. Proliferation and apoptosis of VSMCs were significantly induced in vitro by the downregulation of miR‐145. Also, miR‐145 modulated SMAD3 expression.
Conclusions
miR‐145 was found to be downregulated in patients with AD, which induced the proliferation, migration, and apoptosis of VSMCs by targeting SMAD3. This suggested the involvement of miR‐145 in the pathogenesis of AD.</description><subject>Aged</subject><subject>Aneurysm, Dissecting - genetics</subject><subject>aortic dissection</subject><subject>Apoptosis - genetics</subject><subject>Base Sequence</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>Male</subject><subject>MicroRNAs - blood</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Middle Aged</subject><subject>miR‐145</subject><subject>Muscle, Smooth, Vascular - pathology</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Myocytes, Smooth Muscle - pathology</subject><subject>proliferation</subject><subject>SMAD3</subject><subject>Smad3 Protein - metabolism</subject><subject>vascular smooth muscle cell</subject><issn>0887-8013</issn><issn>1098-2825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><recordid>eNp9kcuKFDEUhoMoTju68QEkSxFrzKUuyUYYGi8jDYLoOpxKnerOkKqUSVXJ7HwEN76gT2KVPT3oxlUO_B_fyeEn5ClnF5wx8eraergQkgl1j2w40yoTShT3yYYpVWWKcXlGHqV0zRhTmpcPyZnkudIV1xvy86qfg5-xw36koaWd-_Tr-w-eF9T1dDwgbXBGH4ZTDiGOztLGpYR2dKGns4OFbSbr-j0dYvCuxQhr9HKx7U8j9A2FIQxjSC6tphmSnTxEmroQxgPtpmQ9Uovep8fkQQs-4ZPb95x8efvm8_Z9tvv47mp7uctsrkqVoQLQivO21LrgXBay4RpaUctcAre1EFjKusmt4A0TiG0NSvAC8zIXhWhBnpPXR-8w1R02djkygjdDdB3EGxPAmX-T3h3MPsym1FUli2oRPL8VxPB1wjSazqX1BOgxTMkIoUotVS5W9MURtTGkFLG9W8OZWXs0a4_mT48L_Ozvj92hp-IWgB-Bb87jzX9U5sN2d3mU_gZM1q1Q</recordid><startdate>202001</startdate><enddate>202001</enddate><creator>Huang, Wenhui</creator><creator>Huang, Cheng</creator><creator>Ding, Huanyu</creator><creator>Luo, Jianfang</creator><creator>Liu, Yuan</creator><creator>Fan, Ruixin</creator><creator>Xiao, Fei</creator><creator>Fan, Xiaoping</creator><creator>Jiang, Zhisheng</creator><general>John Wiley and Sons Inc</general><scope>24P</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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0307-9119</orcidid><orcidid>https://orcid.org/0000-0003-3220-1280</orcidid><orcidid>https://orcid.org/0000-0002-0702-588X</orcidid></search><sort><creationdate>202001</creationdate><title>Involvement of miR‐145 in the development of aortic dissection via inducing proliferation, migration, and apoptosis of vascular smooth muscle cells</title><author>Huang, Wenhui ; Huang, Cheng ; Ding, Huanyu ; Luo, Jianfang ; Liu, Yuan ; Fan, Ruixin ; Xiao, Fei ; Fan, Xiaoping ; Jiang, Zhisheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4868-e8aa9811f699511353d19af2b343a1cb22e63bd4c21d02eefba8215e464252fa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aged</topic><topic>Aneurysm, Dissecting - genetics</topic><topic>aortic dissection</topic><topic>Apoptosis - genetics</topic><topic>Base Sequence</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>Female</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>Male</topic><topic>MicroRNAs - blood</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Middle Aged</topic><topic>miR‐145</topic><topic>Muscle, Smooth, Vascular - pathology</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>Myocytes, Smooth Muscle - pathology</topic><topic>proliferation</topic><topic>SMAD3</topic><topic>Smad3 Protein - metabolism</topic><topic>vascular smooth muscle cell</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Wenhui</creatorcontrib><creatorcontrib>Huang, Cheng</creatorcontrib><creatorcontrib>Ding, Huanyu</creatorcontrib><creatorcontrib>Luo, Jianfang</creatorcontrib><creatorcontrib>Liu, Yuan</creatorcontrib><creatorcontrib>Fan, Ruixin</creatorcontrib><creatorcontrib>Xiao, Fei</creatorcontrib><creatorcontrib>Fan, Xiaoping</creatorcontrib><creatorcontrib>Jiang, Zhisheng</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of clinical laboratory analysis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Wenhui</au><au>Huang, Cheng</au><au>Ding, Huanyu</au><au>Luo, Jianfang</au><au>Liu, Yuan</au><au>Fan, Ruixin</au><au>Xiao, Fei</au><au>Fan, Xiaoping</au><au>Jiang, Zhisheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of miR‐145 in the development of aortic dissection via inducing proliferation, migration, and apoptosis of vascular smooth muscle cells</atitle><jtitle>Journal of clinical laboratory analysis</jtitle><addtitle>J Clin Lab Anal</addtitle><date>2020-01</date><risdate>2020</risdate><volume>34</volume><issue>1</issue><spage>e23028</spage><epage>n/a</epage><pages>e23028-n/a</pages><issn>0887-8013</issn><eissn>1098-2825</eissn><abstract>Aim
The current study aimed to examine miR‐145's contribution to thoracic aortic dissection (AD) development by modulating the biological functions of vascular smooth muscle cells (VSMCs).
Methods
The concentration of circulating miR‐145 was determined in patients with AD and healthy controls using quantitative polymerase chain reaction (qPCR). Aortic specimens were obtained from both individuals with Stanford type A AD undergoing surgical treatment and deceased organ donors (serving as controls) whose causes of death were nonvascular diseases. Then, qPCR and fluorescence in situ hybridization were applied to assess miR‐145 amounts and location, respectively. Furthermore, qPCR and immunoblot were employed to determine SMAD3 (the target gene of miR‐145, involved in the TGF‐β pathway) amounts at the gene and protein levels, respectively. Moreover, in vitro transfection of VSMCs with miR‐145 mimics or inhibitors was conducted. Finally, the 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay, Transwell assay and flow cytometry were employed for detecting VSMC proliferation, migration, and apoptosis, respectively.
Results
The amounts of miR‐145 in plasma and aortic specimens were markedly reduced in the AD group in comparison with control values (P < .05). miR‐145 was mostly located in VSMCs. Proliferation and apoptosis of VSMCs were significantly induced in vitro by the downregulation of miR‐145. Also, miR‐145 modulated SMAD3 expression.
Conclusions
miR‐145 was found to be downregulated in patients with AD, which induced the proliferation, migration, and apoptosis of VSMCs by targeting SMAD3. This suggested the involvement of miR‐145 in the pathogenesis of AD.</abstract><cop>United States</cop><pub>John Wiley and Sons Inc</pub><pmid>31489719</pmid><doi>10.1002/jcla.23028</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-0307-9119</orcidid><orcidid>https://orcid.org/0000-0003-3220-1280</orcidid><orcidid>https://orcid.org/0000-0002-0702-588X</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Online Library Open Access; DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Aged Aneurysm, Dissecting - genetics aortic dissection Apoptosis - genetics Base Sequence Cell Movement - genetics Cell Proliferation - genetics Female Gene Expression Regulation Humans Male MicroRNAs - blood MicroRNAs - genetics MicroRNAs - metabolism Middle Aged miR‐145 Muscle, Smooth, Vascular - pathology Myocytes, Smooth Muscle - metabolism Myocytes, Smooth Muscle - pathology proliferation SMAD3 Smad3 Protein - metabolism vascular smooth muscle cell |
| title | Involvement of miR‐145 in the development of aortic dissection via inducing proliferation, migration, and apoptosis of vascular smooth muscle cells |
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