The Anti-fibrotic Effects and Mechanisms of MicroRNA-486-5p in Pulmonary Fibrosis
To identify microRNAs (miRNAs, miRs) with potential roles in lung fibrogenesis, we performed genome-wide profiling of miRNA expression in lung tissues from a silica-induced mouse model of pulmonary fibrosis using microarrays. Seventeen miRNAs were selected for validation via qRT-PCR based on the fol...
Gespeichert in:
| Veröffentlicht in: | Scientific reports 2015-09, Vol.5 (1), p.14131-14131, Article 14131 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 14131 |
|---|---|
| container_issue | 1 |
| container_start_page | 14131 |
| container_title | Scientific reports |
| container_volume | 5 |
| creator | Ji, Xiaoming Wu, Baiqun Fan, Jingjing Han, Ruhui Luo, Chen Wang, Ting Yang, Jingjin Han, Lei Zhu, Baoli Wei, Dong Chen, Jingyu Ni, Chunhui |
| description | To identify microRNAs (miRNAs, miRs) with potential roles in lung fibrogenesis, we performed genome-wide profiling of miRNA expression in lung tissues from a silica-induced mouse model of pulmonary fibrosis using microarrays. Seventeen miRNAs were selected for validation via qRT-PCR based on the fold changes between the silica and the control group. The dysregulation of five miRNAs, including miR-21, miR-455, miR-151-3p, miR-486-5p and miR-3107, were confirmed by qRT-PCRs in silica-induced mouse model of pulmonary fibrosis and were also confirmed in a bleomycin (BLM)-induced mouse lung fibrosis. Notably, miR-486-5p levels were decreased in the serum samples of patients with silicosis, as well as in the lung tissues of patients with silicosis and idiopathic pulmonary fibrosis (IPF). In addition, as determined by luciferase assays and Western blotting, SMAD2, a crucial mediator of pulmonary fibrosis, was identified to be one of target genes of miR-486-5p. To test the potential therapeutic significance of this miRNA, we overexpressed miR-486-5p in animal models. At day 28, miR-486-5p expression significantly decreased both the distribution and severity of lung lesions compared with the silica group (
P
|
| doi_str_mv | 10.1038/srep14131 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4569899</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1899747898</sourcerecordid><originalsourceid>FETCH-LOGICAL-c504t-59e11bbc396f975178086a898ab18d0a45b2caba9fac614d05b044e237441ab73</originalsourceid><addsrcrecordid>eNplkV9rHCEUxSU0JCHJQ79AEPLSFqb1OjrqS2EJSRNI-o_0WdR1soYZ3ehMod--hk2XbeuLwv157rn3IPQayHsgrfxQsl8Dgxb20BEljDe0pfTVzvsQnZbySOrhVDFQB-iQdq0gHfAj9O1-5fEiTqHpg81pCg5f9r13U8EmLvGddysTQxkLTj2-Cy6n758XDZNdw9c4RPx1HsYUTf6Fr57_l1BO0H5vhuJPX-5j9OPq8v7iurn98unmYnHbOE7Y1HDlAax1rep6JTgISWRnpJLGglwSw7ilzlijeuM6YEvCLWHM01YwBsaK9hh93OiuZzv6pfNxymbQ6xzGakcnE_TflRhW-iH91Ix3SipVBd68COT0NPsy6TEU54fBRJ_mokEAFUJ1klb0_B_0Mc051vE0VCnBRDVeqbcbqm6p1Fj6rRkg-jkrvc2qsme77rfkn2Qq8G4DlFqKDz7vtPxP7TezAZv8</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1899747898</pqid></control><display><type>article</type><title>The Anti-fibrotic Effects and Mechanisms of MicroRNA-486-5p in Pulmonary Fibrosis</title><source>MEDLINE</source><source>Nature Free</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>Free Full-Text Journals in Chemistry</source><source>Springer Nature OA Free Journals</source><creator>Ji, Xiaoming ; Wu, Baiqun ; Fan, Jingjing ; Han, Ruhui ; Luo, Chen ; Wang, Ting ; Yang, Jingjin ; Han, Lei ; Zhu, Baoli ; Wei, Dong ; Chen, Jingyu ; Ni, Chunhui</creator><creatorcontrib>Ji, Xiaoming ; Wu, Baiqun ; Fan, Jingjing ; Han, Ruhui ; Luo, Chen ; Wang, Ting ; Yang, Jingjin ; Han, Lei ; Zhu, Baoli ; Wei, Dong ; Chen, Jingyu ; Ni, Chunhui</creatorcontrib><description>To identify microRNAs (miRNAs, miRs) with potential roles in lung fibrogenesis, we performed genome-wide profiling of miRNA expression in lung tissues from a silica-induced mouse model of pulmonary fibrosis using microarrays. Seventeen miRNAs were selected for validation via qRT-PCR based on the fold changes between the silica and the control group. The dysregulation of five miRNAs, including miR-21, miR-455, miR-151-3p, miR-486-5p and miR-3107, were confirmed by qRT-PCRs in silica-induced mouse model of pulmonary fibrosis and were also confirmed in a bleomycin (BLM)-induced mouse lung fibrosis. Notably, miR-486-5p levels were decreased in the serum samples of patients with silicosis, as well as in the lung tissues of patients with silicosis and idiopathic pulmonary fibrosis (IPF). In addition, as determined by luciferase assays and Western blotting, SMAD2, a crucial mediator of pulmonary fibrosis, was identified to be one of target genes of miR-486-5p. To test the potential therapeutic significance of this miRNA, we overexpressed miR-486-5p in animal models. At day 28, miR-486-5p expression significantly decreased both the distribution and severity of lung lesions compared with the silica group (
P
< 0.01). In addition, miR-486-5p had a similar effect in the BLM group (
P
< 0.001). These results indicate that miR-486-5p may inhibit fibrosis.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep14131</identifier><identifier>PMID: 26370615</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/337 ; 631/337/384/331 ; Animal models ; Animals ; Base Sequence ; Binding Sites ; Bleomycin ; Cell Proliferation - drug effects ; Chromosome 5 ; Disease Models, Animal ; Down-Regulation ; Fibroblasts - drug effects ; Fibroblasts - metabolism ; Fibrosis ; Gene Expression Regulation - drug effects ; Genomes ; Humanities and Social Sciences ; Humans ; Lung - metabolism ; Lung - pathology ; Lung diseases ; Mice ; MicroRNAs - chemistry ; MicroRNAs - genetics ; miRNA ; multidisciplinary ; Polymerase chain reaction ; Pulmonary fibrosis ; Pulmonary Fibrosis - genetics ; Pulmonary Fibrosis - pathology ; RNA Interference ; Rodents ; Science ; Silica ; Silicosis ; Silicosis - genetics ; Silicosis - pathology ; Smad2 protein ; Smad2 Protein - chemistry ; Smad2 Protein - genetics ; Transforming Growth Factor beta1 - pharmacology ; Western blotting</subject><ispartof>Scientific reports, 2015-09, Vol.5 (1), p.14131-14131, Article 14131</ispartof><rights>The Author(s) 2015</rights><rights>Copyright Nature Publishing Group Sep 2015</rights><rights>Copyright © 2015, Macmillan Publishers Limited 2015 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-59e11bbc396f975178086a898ab18d0a45b2caba9fac614d05b044e237441ab73</citedby><cites>FETCH-LOGICAL-c504t-59e11bbc396f975178086a898ab18d0a45b2caba9fac614d05b044e237441ab73</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/PMC4569899/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4569899/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26370615$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ji, Xiaoming</creatorcontrib><creatorcontrib>Wu, Baiqun</creatorcontrib><creatorcontrib>Fan, Jingjing</creatorcontrib><creatorcontrib>Han, Ruhui</creatorcontrib><creatorcontrib>Luo, Chen</creatorcontrib><creatorcontrib>Wang, Ting</creatorcontrib><creatorcontrib>Yang, Jingjin</creatorcontrib><creatorcontrib>Han, Lei</creatorcontrib><creatorcontrib>Zhu, Baoli</creatorcontrib><creatorcontrib>Wei, Dong</creatorcontrib><creatorcontrib>Chen, Jingyu</creatorcontrib><creatorcontrib>Ni, Chunhui</creatorcontrib><title>The Anti-fibrotic Effects and Mechanisms of MicroRNA-486-5p in Pulmonary Fibrosis</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>To identify microRNAs (miRNAs, miRs) with potential roles in lung fibrogenesis, we performed genome-wide profiling of miRNA expression in lung tissues from a silica-induced mouse model of pulmonary fibrosis using microarrays. Seventeen miRNAs were selected for validation via qRT-PCR based on the fold changes between the silica and the control group. The dysregulation of five miRNAs, including miR-21, miR-455, miR-151-3p, miR-486-5p and miR-3107, were confirmed by qRT-PCRs in silica-induced mouse model of pulmonary fibrosis and were also confirmed in a bleomycin (BLM)-induced mouse lung fibrosis. Notably, miR-486-5p levels were decreased in the serum samples of patients with silicosis, as well as in the lung tissues of patients with silicosis and idiopathic pulmonary fibrosis (IPF). In addition, as determined by luciferase assays and Western blotting, SMAD2, a crucial mediator of pulmonary fibrosis, was identified to be one of target genes of miR-486-5p. To test the potential therapeutic significance of this miRNA, we overexpressed miR-486-5p in animal models. At day 28, miR-486-5p expression significantly decreased both the distribution and severity of lung lesions compared with the silica group (
P
< 0.01). In addition, miR-486-5p had a similar effect in the BLM group (
P
< 0.001). These results indicate that miR-486-5p may inhibit fibrosis.</description><subject>631/337</subject><subject>631/337/384/331</subject><subject>Animal models</subject><subject>Animals</subject><subject>Base Sequence</subject><subject>Binding Sites</subject><subject>Bleomycin</subject><subject>Cell Proliferation - drug effects</subject><subject>Chromosome 5</subject><subject>Disease Models, Animal</subject><subject>Down-Regulation</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - metabolism</subject><subject>Fibrosis</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Genomes</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Lung - metabolism</subject><subject>Lung - pathology</subject><subject>Lung diseases</subject><subject>Mice</subject><subject>MicroRNAs - chemistry</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>multidisciplinary</subject><subject>Polymerase chain reaction</subject><subject>Pulmonary fibrosis</subject><subject>Pulmonary Fibrosis - genetics</subject><subject>Pulmonary Fibrosis - pathology</subject><subject>RNA Interference</subject><subject>Rodents</subject><subject>Science</subject><subject>Silica</subject><subject>Silicosis</subject><subject>Silicosis - genetics</subject><subject>Silicosis - pathology</subject><subject>Smad2 protein</subject><subject>Smad2 Protein - chemistry</subject><subject>Smad2 Protein - genetics</subject><subject>Transforming Growth Factor beta1 - pharmacology</subject><subject>Western blotting</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNplkV9rHCEUxSU0JCHJQ79AEPLSFqb1OjrqS2EJSRNI-o_0WdR1soYZ3ehMod--hk2XbeuLwv157rn3IPQayHsgrfxQsl8Dgxb20BEljDe0pfTVzvsQnZbySOrhVDFQB-iQdq0gHfAj9O1-5fEiTqHpg81pCg5f9r13U8EmLvGddysTQxkLTj2-Cy6n758XDZNdw9c4RPx1HsYUTf6Fr57_l1BO0H5vhuJPX-5j9OPq8v7iurn98unmYnHbOE7Y1HDlAax1rep6JTgISWRnpJLGglwSw7ilzlijeuM6YEvCLWHM01YwBsaK9hh93OiuZzv6pfNxymbQ6xzGakcnE_TflRhW-iH91Ix3SipVBd68COT0NPsy6TEU54fBRJ_mokEAFUJ1klb0_B_0Mc051vE0VCnBRDVeqbcbqm6p1Fj6rRkg-jkrvc2qsme77rfkn2Qq8G4DlFqKDz7vtPxP7TezAZv8</recordid><startdate>20150915</startdate><enddate>20150915</enddate><creator>Ji, Xiaoming</creator><creator>Wu, Baiqun</creator><creator>Fan, Jingjing</creator><creator>Han, Ruhui</creator><creator>Luo, Chen</creator><creator>Wang, Ting</creator><creator>Yang, Jingjin</creator><creator>Han, Lei</creator><creator>Zhu, Baoli</creator><creator>Wei, Dong</creator><creator>Chen, Jingyu</creator><creator>Ni, Chunhui</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</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>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150915</creationdate><title>The Anti-fibrotic Effects and Mechanisms of MicroRNA-486-5p in Pulmonary Fibrosis</title><author>Ji, Xiaoming ; Wu, Baiqun ; Fan, Jingjing ; Han, Ruhui ; Luo, Chen ; Wang, Ting ; Yang, Jingjin ; Han, Lei ; Zhu, Baoli ; Wei, Dong ; Chen, Jingyu ; Ni, Chunhui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-59e11bbc396f975178086a898ab18d0a45b2caba9fac614d05b044e237441ab73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>631/337</topic><topic>631/337/384/331</topic><topic>Animal models</topic><topic>Animals</topic><topic>Base Sequence</topic><topic>Binding Sites</topic><topic>Bleomycin</topic><topic>Cell Proliferation - drug effects</topic><topic>Chromosome 5</topic><topic>Disease Models, Animal</topic><topic>Down-Regulation</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - metabolism</topic><topic>Fibrosis</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Genomes</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Lung - metabolism</topic><topic>Lung - pathology</topic><topic>Lung diseases</topic><topic>Mice</topic><topic>MicroRNAs - chemistry</topic><topic>MicroRNAs - genetics</topic><topic>miRNA</topic><topic>multidisciplinary</topic><topic>Polymerase chain reaction</topic><topic>Pulmonary fibrosis</topic><topic>Pulmonary Fibrosis - genetics</topic><topic>Pulmonary Fibrosis - pathology</topic><topic>RNA Interference</topic><topic>Rodents</topic><topic>Science</topic><topic>Silica</topic><topic>Silicosis</topic><topic>Silicosis - genetics</topic><topic>Silicosis - pathology</topic><topic>Smad2 protein</topic><topic>Smad2 Protein - chemistry</topic><topic>Smad2 Protein - genetics</topic><topic>Transforming Growth Factor beta1 - pharmacology</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ji, Xiaoming</creatorcontrib><creatorcontrib>Wu, Baiqun</creatorcontrib><creatorcontrib>Fan, Jingjing</creatorcontrib><creatorcontrib>Han, Ruhui</creatorcontrib><creatorcontrib>Luo, Chen</creatorcontrib><creatorcontrib>Wang, Ting</creatorcontrib><creatorcontrib>Yang, Jingjin</creatorcontrib><creatorcontrib>Han, Lei</creatorcontrib><creatorcontrib>Zhu, Baoli</creatorcontrib><creatorcontrib>Wei, Dong</creatorcontrib><creatorcontrib>Chen, Jingyu</creatorcontrib><creatorcontrib>Ni, Chunhui</creatorcontrib><collection>Springer Nature OA Free Journals</collection><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>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</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 Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</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 Korea</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>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ji, Xiaoming</au><au>Wu, Baiqun</au><au>Fan, Jingjing</au><au>Han, Ruhui</au><au>Luo, Chen</au><au>Wang, Ting</au><au>Yang, Jingjin</au><au>Han, Lei</au><au>Zhu, Baoli</au><au>Wei, Dong</au><au>Chen, Jingyu</au><au>Ni, Chunhui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Anti-fibrotic Effects and Mechanisms of MicroRNA-486-5p in Pulmonary Fibrosis</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2015-09-15</date><risdate>2015</risdate><volume>5</volume><issue>1</issue><spage>14131</spage><epage>14131</epage><pages>14131-14131</pages><artnum>14131</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>To identify microRNAs (miRNAs, miRs) with potential roles in lung fibrogenesis, we performed genome-wide profiling of miRNA expression in lung tissues from a silica-induced mouse model of pulmonary fibrosis using microarrays. Seventeen miRNAs were selected for validation via qRT-PCR based on the fold changes between the silica and the control group. The dysregulation of five miRNAs, including miR-21, miR-455, miR-151-3p, miR-486-5p and miR-3107, were confirmed by qRT-PCRs in silica-induced mouse model of pulmonary fibrosis and were also confirmed in a bleomycin (BLM)-induced mouse lung fibrosis. Notably, miR-486-5p levels were decreased in the serum samples of patients with silicosis, as well as in the lung tissues of patients with silicosis and idiopathic pulmonary fibrosis (IPF). In addition, as determined by luciferase assays and Western blotting, SMAD2, a crucial mediator of pulmonary fibrosis, was identified to be one of target genes of miR-486-5p. To test the potential therapeutic significance of this miRNA, we overexpressed miR-486-5p in animal models. At day 28, miR-486-5p expression significantly decreased both the distribution and severity of lung lesions compared with the silica group (
P
< 0.01). In addition, miR-486-5p had a similar effect in the BLM group (
P
< 0.001). These results indicate that miR-486-5p may inhibit fibrosis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>26370615</pmid><doi>10.1038/srep14131</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2045-2322 |
| ispartof | Scientific reports, 2015-09, Vol.5 (1), p.14131-14131, Article 14131 |
| issn | 2045-2322 2045-2322 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4569899 |
| source | MEDLINE; Nature Free; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry; Springer Nature OA Free Journals |
| subjects | 631/337 631/337/384/331 Animal models Animals Base Sequence Binding Sites Bleomycin Cell Proliferation - drug effects Chromosome 5 Disease Models, Animal Down-Regulation Fibroblasts - drug effects Fibroblasts - metabolism Fibrosis Gene Expression Regulation - drug effects Genomes Humanities and Social Sciences Humans Lung - metabolism Lung - pathology Lung diseases Mice MicroRNAs - chemistry MicroRNAs - genetics miRNA multidisciplinary Polymerase chain reaction Pulmonary fibrosis Pulmonary Fibrosis - genetics Pulmonary Fibrosis - pathology RNA Interference Rodents Science Silica Silicosis Silicosis - genetics Silicosis - pathology Smad2 protein Smad2 Protein - chemistry Smad2 Protein - genetics Transforming Growth Factor beta1 - pharmacology Western blotting |
| title | The Anti-fibrotic Effects and Mechanisms of MicroRNA-486-5p in Pulmonary Fibrosis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-05T04%3A51%3A43IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20Anti-fibrotic%20Effects%20and%20Mechanisms%20of%20MicroRNA-486-5p%20in%20Pulmonary%20Fibrosis&rft.jtitle=Scientific%20reports&rft.au=Ji,%20Xiaoming&rft.date=2015-09-15&rft.volume=5&rft.issue=1&rft.spage=14131&rft.epage=14131&rft.pages=14131-14131&rft.artnum=14131&rft.issn=2045-2322&rft.eissn=2045-2322&rft_id=info:doi/10.1038/srep14131&rft_dat=%3Cproquest_pubme%3E1899747898%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1899747898&rft_id=info:pmid/26370615&rfr_iscdi=true |