The tissue specific regulation of miR22 expression in the lung and brain by ribosomal protein L29
Endogenous miR22 is associated with a diverse range of biological processes through post-translational modification of gene expression and its deregulation results in various diseases including cancer. Its expression is usually tissue or cell-specific, however, the reasons behind this tissue or cell...
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description | Endogenous miR22 is associated with a diverse range of biological processes through post-translational modification of gene expression and its deregulation results in various diseases including cancer. Its expression is usually tissue or cell-specific, however, the reasons behind this tissue or cell specificity are not clearly outlined till-date. Therefore, our keen interest was to investigate the mechanisms of tissue or cell-specific expression of miR22. In the current study, miR22 expression showed a tissues-specific difference in the poly(I:C) induced inflammatory mouse lung and brain tissues. The cell-specific different expression of miR22 was also observed in inflammatory glial cells and endothelial cells. The pattern of RPL29 expression was also similar to miR22 in these tissues and cells under the same treatment. Interestingly, the knockdown of RPL29 exerted an inhibitory effect on miR22 and its known transcription factors including Fos-B and c-Fos. Fos-B and c-Fos were also differentially expressed in the two cell lines transfected with poly(I:C). The knockdown of c-Fos also exerted its negative effects on miR22 expression in both cells. These findings suggest that RPL29 might have regulatory roles on tissue or cell-specific expression of miR22 through the transcription activities of c-Fos and also possibly through Fos-B. |
doi_str_mv | 10.1038/s41598-020-73281-z |
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Its expression is usually tissue or cell-specific, however, the reasons behind this tissue or cell specificity are not clearly outlined till-date. Therefore, our keen interest was to investigate the mechanisms of tissue or cell-specific expression of miR22. In the current study, miR22 expression showed a tissues-specific difference in the poly(I:C) induced inflammatory mouse lung and brain tissues. The cell-specific different expression of miR22 was also observed in inflammatory glial cells and endothelial cells. The pattern of RPL29 expression was also similar to miR22 in these tissues and cells under the same treatment. Interestingly, the knockdown of RPL29 exerted an inhibitory effect on miR22 and its known transcription factors including Fos-B and c-Fos. Fos-B and c-Fos were also differentially expressed in the two cell lines transfected with poly(I:C). The knockdown of c-Fos also exerted its negative effects on miR22 expression in both cells. These findings suggest that RPL29 might have regulatory roles on tissue or cell-specific expression of miR22 through the transcription activities of c-Fos and also possibly through Fos-B.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-020-73281-z</identifier><identifier>PMID: 33004906</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/337 ; 631/45 ; 631/80 ; Animals ; Brain - metabolism ; c-Fos protein ; Cell Line ; Deregulation ; Endothelial cells ; Gene expression ; Gene Expression Regulation ; Glial cells ; Humanities and Social Sciences ; Humans ; Inflammation ; Lung - metabolism ; Male ; Mice ; Mice, Inbred C57BL ; MicroRNAs - metabolism ; multidisciplinary ; Polyinosinic:polycytidylic acid ; Post-translation ; Real-Time Polymerase Chain Reaction ; Ribosomal protein L29 ; Ribosomal Proteins - metabolism ; RNA-Binding Proteins - metabolism ; Science ; Science (multidisciplinary) ; Tissues ; Transcription factors</subject><ispartof>Scientific reports, 2020-10, Vol.10 (1), p.16242-16242, Article 16242</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. 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Its expression is usually tissue or cell-specific, however, the reasons behind this tissue or cell specificity are not clearly outlined till-date. Therefore, our keen interest was to investigate the mechanisms of tissue or cell-specific expression of miR22. In the current study, miR22 expression showed a tissues-specific difference in the poly(I:C) induced inflammatory mouse lung and brain tissues. The cell-specific different expression of miR22 was also observed in inflammatory glial cells and endothelial cells. The pattern of RPL29 expression was also similar to miR22 in these tissues and cells under the same treatment. Interestingly, the knockdown of RPL29 exerted an inhibitory effect on miR22 and its known transcription factors including Fos-B and c-Fos. Fos-B and c-Fos were also differentially expressed in the two cell lines transfected with poly(I:C). The knockdown of c-Fos also exerted its negative effects on miR22 expression in both cells. These findings suggest that RPL29 might have regulatory roles on tissue or cell-specific expression of miR22 through the transcription activities of c-Fos and also possibly through Fos-B.</description><subject>631/337</subject><subject>631/45</subject><subject>631/80</subject><subject>Animals</subject><subject>Brain - metabolism</subject><subject>c-Fos protein</subject><subject>Cell Line</subject><subject>Deregulation</subject><subject>Endothelial cells</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Glial cells</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Lung - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>MicroRNAs - metabolism</subject><subject>multidisciplinary</subject><subject>Polyinosinic:polycytidylic acid</subject><subject>Post-translation</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Ribosomal protein L29</subject><subject>Ribosomal Proteins - metabolism</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Tissues</subject><subject>Transcription factors</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kU9LHTEUxUOxVLF-gS4k4MbNtDf_3sxshCJqCw8Kxa5DJnPzjMwkYzJT1E9vXp-1totmc8O5v3uSyyHkA4OPDETzKUum2qYCDlUteMOqxzfkgINUFRec772675OjnG-hHMVbydp3ZF8IANnC6oCY6xuks895QZontN55SxNulsHMPgYaHR39d84p3k8Jc95qPtC5TA1L2FATetolU6TugSbfxRxHM9ApxRmLuObte_LWmSHj0XM9JD8uL67Pv1Trb1dfzz-vK6sYm6vGGbCqY8pgWztTQ927Umyv-r4RCAYYVxasVI3ogDthTK2albXKua4TTBySs53vtHQj9hbDnMygp-RHkx50NF7_3Qn-Rm_iT10rAcWqGJw-G6R4t2Ce9eizxWEwAeOSNZeykSD5aoue_IPexiWFst6WaqUStRSF4jvKpphzQvfyGQZ6G6LehahLiPpXiPqxDB2_XuNl5HdkBRA7IJdW2GD68_Z_bJ8ApiypQw</recordid><startdate>20201001</startdate><enddate>20201001</enddate><creator>Ali, Mohammad Ishaque</creator><creator>Li, Linrui</creator><creator>Li, Lexing</creator><creator>Yao, Lun</creator><creator>Liu, Jie</creator><creator>Gu, Wei</creator><creator>Huang, Shuguang</creator><creator>Wang, Bingyu</creator><creator>Liu, Guoquan</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>20201001</creationdate><title>The tissue specific regulation of miR22 expression in the lung and brain by ribosomal protein L29</title><author>Ali, Mohammad Ishaque ; Li, Linrui ; Li, Lexing ; Yao, Lun ; Liu, Jie ; Gu, Wei ; Huang, Shuguang ; Wang, Bingyu ; Liu, Guoquan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c511t-8fa0c5b15ae97fa707dffa7cd5dd83e0a0125c0c4583b02f3aa7586cc5ffbb313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>631/337</topic><topic>631/45</topic><topic>631/80</topic><topic>Animals</topic><topic>Brain - metabolism</topic><topic>c-Fos protein</topic><topic>Cell Line</topic><topic>Deregulation</topic><topic>Endothelial cells</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Glial cells</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Lung - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>MicroRNAs - metabolism</topic><topic>multidisciplinary</topic><topic>Polyinosinic:polycytidylic acid</topic><topic>Post-translation</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Ribosomal protein L29</topic><topic>Ribosomal Proteins - metabolism</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Tissues</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ali, Mohammad Ishaque</creatorcontrib><creatorcontrib>Li, Linrui</creatorcontrib><creatorcontrib>Li, Lexing</creatorcontrib><creatorcontrib>Yao, Lun</creatorcontrib><creatorcontrib>Liu, Jie</creatorcontrib><creatorcontrib>Gu, Wei</creatorcontrib><creatorcontrib>Huang, Shuguang</creatorcontrib><creatorcontrib>Wang, Bingyu</creatorcontrib><creatorcontrib>Liu, Guoquan</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>Ali, Mohammad Ishaque</au><au>Li, Linrui</au><au>Li, Lexing</au><au>Yao, Lun</au><au>Liu, Jie</au><au>Gu, Wei</au><au>Huang, Shuguang</au><au>Wang, Bingyu</au><au>Liu, Guoquan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The tissue specific regulation of miR22 expression in the lung and brain by ribosomal protein L29</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2020-10-01</date><risdate>2020</risdate><volume>10</volume><issue>1</issue><spage>16242</spage><epage>16242</epage><pages>16242-16242</pages><artnum>16242</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Endogenous miR22 is associated with a diverse range of biological processes through post-translational modification of gene expression and its deregulation results in various diseases including cancer. Its expression is usually tissue or cell-specific, however, the reasons behind this tissue or cell specificity are not clearly outlined till-date. Therefore, our keen interest was to investigate the mechanisms of tissue or cell-specific expression of miR22. In the current study, miR22 expression showed a tissues-specific difference in the poly(I:C) induced inflammatory mouse lung and brain tissues. The cell-specific different expression of miR22 was also observed in inflammatory glial cells and endothelial cells. The pattern of RPL29 expression was also similar to miR22 in these tissues and cells under the same treatment. Interestingly, the knockdown of RPL29 exerted an inhibitory effect on miR22 and its known transcription factors including Fos-B and c-Fos. Fos-B and c-Fos were also differentially expressed in the two cell lines transfected with poly(I:C). The knockdown of c-Fos also exerted its negative effects on miR22 expression in both cells. These findings suggest that RPL29 might have regulatory roles on tissue or cell-specific expression of miR22 through the transcription activities of c-Fos and also possibly through Fos-B.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>33004906</pmid><doi>10.1038/s41598-020-73281-z</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 631/337 631/45 631/80 Animals Brain - metabolism c-Fos protein Cell Line Deregulation Endothelial cells Gene expression Gene Expression Regulation Glial cells Humanities and Social Sciences Humans Inflammation Lung - metabolism Male Mice Mice, Inbred C57BL MicroRNAs - metabolism multidisciplinary Polyinosinic:polycytidylic acid Post-translation Real-Time Polymerase Chain Reaction Ribosomal protein L29 Ribosomal Proteins - metabolism RNA-Binding Proteins - metabolism Science Science (multidisciplinary) Tissues Transcription factors |
title | The tissue specific regulation of miR22 expression in the lung and brain by ribosomal protein L29 |
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