Silencing circular ANRIL protects HK-2 cells from lipopolysaccharide-induced inflammatory injury through up-regulating microRNA-9
Circular antisense non-coding RNA in the INK4 locus (cANRIL) participated in inflammation of endothelial cells. However, whether cANRIL is associated with inflammatory injury of HK-2 cells, thereby affecting chronic kidney disease has not been investigated. We tested the hypothesis that cANRIL parti...
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| description | Circular antisense non-coding RNA in the INK4 locus (cANRIL) participated in inflammation of endothelial cells. However, whether cANRIL is associated with inflammatory injury of HK-2 cells, thereby affecting chronic kidney disease has not been investigated. We tested the hypothesis that cANRIL participated in inflammatory response in vitro. HK-2 cells were stimulated by lipopolysaccharides (LPS). RT-qPCR was executed for cANRIL expression assessment. After transfection, cell viability, apoptosis, inflammatory cytokines and ROS generation were appraised to evaluate the impact of silencing cANRIL on LPS-induced inflammatory injury. The regulatory relationship between cANRIL and microRNA-9 (miR-9) was verified. In addition, whether miR-9 affected LPS-induced inflammatory injury was measured after miR-9 inhibitor transfection. Western blot was utilized to detect NF-κB and JNK/p38 pathway-related proteins. The results showed that LPS promoted cANRIL expression and cell injuries in HK-2 cells. Furthermore, silencing cANRIL alleviated inflammatory injuries by promoting viability, suppressing apoptosis, inflammatory cytokines and ROS generation in HK-2 cells. In addition, miR-9 expression was accelerated by silencing cANRIL. Meanwhile, miR-9 down-regulation invalidated the effect of silencing cANRIL on inflammation and NF-κB and JNK/p38 pathways. The study clarified that silencing cANRIL hindered NF-κB and JNK/p38 pathways by positively regulating miR-9, thereby protecting HK-2 cells from LPS-induced injury. |
| doi_str_mv | 10.1080/21691401.2019.1652187 |
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However, whether cANRIL is associated with inflammatory injury of HK-2 cells, thereby affecting chronic kidney disease has not been investigated. We tested the hypothesis that cANRIL participated in inflammatory response in vitro. HK-2 cells were stimulated by lipopolysaccharides (LPS). RT-qPCR was executed for cANRIL expression assessment. After transfection, cell viability, apoptosis, inflammatory cytokines and ROS generation were appraised to evaluate the impact of silencing cANRIL on LPS-induced inflammatory injury. The regulatory relationship between cANRIL and microRNA-9 (miR-9) was verified. In addition, whether miR-9 affected LPS-induced inflammatory injury was measured after miR-9 inhibitor transfection. Western blot was utilized to detect NF-κB and JNK/p38 pathway-related proteins. The results showed that LPS promoted cANRIL expression and cell injuries in HK-2 cells. Furthermore, silencing cANRIL alleviated inflammatory injuries by promoting viability, suppressing apoptosis, inflammatory cytokines and ROS generation in HK-2 cells. In addition, miR-9 expression was accelerated by silencing cANRIL. Meanwhile, miR-9 down-regulation invalidated the effect of silencing cANRIL on inflammation and NF-κB and JNK/p38 pathways. The study clarified that silencing cANRIL hindered NF-κB and JNK/p38 pathways by positively regulating miR-9, thereby protecting HK-2 cells from LPS-induced injury.</description><identifier>ISSN: 2169-1401</identifier><identifier>EISSN: 2169-141X</identifier><identifier>DOI: 10.1080/21691401.2019.1652187</identifier><identifier>PMID: 31432701</identifier><language>eng</language><publisher>England: Taylor & Francis</publisher><subject>Antisense RNA ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; Cell Line, Tumor ; Cell viability ; Chronic kidney disease ; circular ANRIL ; Cyclin-dependent kinase inhibitors ; Cytokines ; Endothelial cells ; Gene Expression Regulation, Neoplastic - drug effects ; Gene Expression Regulation, Neoplastic - genetics ; Gene Silencing ; Humans ; Inflammation ; Inflammation - chemically induced ; Inflammation - genetics ; Inflammation - pathology ; Inflammatory response ; Injuries ; INK4 protein ; JNK Mitogen-Activated Protein Kinases - metabolism ; Kidney diseases ; lipopolysaccharide ; Lipopolysaccharides ; Lipopolysaccharides - pharmacology ; microRNA-9 ; MicroRNAs ; MicroRNAs - genetics ; miRNA ; NF-kappa B - metabolism ; NF-κB protein ; Non-coding RNA ; p38 Mitogen-Activated Protein Kinases - metabolism ; Ribonucleic acid ; RNA ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Signal Transduction - drug effects ; Signal Transduction - genetics ; Transfection ; Up-Regulation - drug effects ; Up-Regulation - genetics</subject><ispartof>Artificial cells, nanomedicine, and biotechnology, 2019-12, Vol.47 (1), p.3478-3484</ispartof><rights>2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2019</rights><rights>2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This work is licensed under the Creative Commons Attribution – Non-Commercial License http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c507t-1df220d221c8e158cd7b8609db348ba8dbfa1c65032673db29251e6ae71ab3293</citedby><cites>FETCH-LOGICAL-c507t-1df220d221c8e158cd7b8609db348ba8dbfa1c65032673db29251e6ae71ab3293</cites><orcidid>0000-0002-3457-5393</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,2101,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31432701$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Deng, Wenyan</creatorcontrib><creatorcontrib>Chen, Kai</creatorcontrib><creatorcontrib>Liu, Shuxia</creatorcontrib><creatorcontrib>Wang, Yingying</creatorcontrib><title>Silencing circular ANRIL protects HK-2 cells from lipopolysaccharide-induced inflammatory injury through up-regulating microRNA-9</title><title>Artificial cells, nanomedicine, and biotechnology</title><addtitle>Artif Cells Nanomed Biotechnol</addtitle><description>Circular antisense non-coding RNA in the INK4 locus (cANRIL) participated in inflammation of endothelial cells. However, whether cANRIL is associated with inflammatory injury of HK-2 cells, thereby affecting chronic kidney disease has not been investigated. We tested the hypothesis that cANRIL participated in inflammatory response in vitro. HK-2 cells were stimulated by lipopolysaccharides (LPS). RT-qPCR was executed for cANRIL expression assessment. After transfection, cell viability, apoptosis, inflammatory cytokines and ROS generation were appraised to evaluate the impact of silencing cANRIL on LPS-induced inflammatory injury. The regulatory relationship between cANRIL and microRNA-9 (miR-9) was verified. In addition, whether miR-9 affected LPS-induced inflammatory injury was measured after miR-9 inhibitor transfection. Western blot was utilized to detect NF-κB and JNK/p38 pathway-related proteins. The results showed that LPS promoted cANRIL expression and cell injuries in HK-2 cells. Furthermore, silencing cANRIL alleviated inflammatory injuries by promoting viability, suppressing apoptosis, inflammatory cytokines and ROS generation in HK-2 cells. In addition, miR-9 expression was accelerated by silencing cANRIL. Meanwhile, miR-9 down-regulation invalidated the effect of silencing cANRIL on inflammation and NF-κB and JNK/p38 pathways. The study clarified that silencing cANRIL hindered NF-κB and JNK/p38 pathways by positively regulating miR-9, thereby protecting HK-2 cells from LPS-induced injury.</description><subject>Antisense RNA</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cell viability</subject><subject>Chronic kidney disease</subject><subject>circular ANRIL</subject><subject>Cyclin-dependent kinase inhibitors</subject><subject>Cytokines</subject><subject>Endothelial cells</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Gene Silencing</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - genetics</subject><subject>Inflammation - pathology</subject><subject>Inflammatory response</subject><subject>Injuries</subject><subject>INK4 protein</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Kidney diseases</subject><subject>lipopolysaccharide</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>microRNA-9</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Non-coding RNA</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - genetics</subject><subject>Transfection</subject><subject>Up-Regulation - drug effects</subject><subject>Up-Regulation - genetics</subject><issn>2169-1401</issn><issn>2169-141X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>EIF</sourceid><sourceid>DOA</sourceid><recordid>eNp9Uctu2zAQFIoWTZDkE1oI6Fkul3qQutUImsaokQBpAvRGLB-yaVCiSkoofOyfl64dH8vLchezM-RMln0AsgDCyWcKTQsVgQUl0C6gqSlw9ia7PMwLqODn2_OdwEV2E-OOpMOhYXX1PrsooSopI3CZ_flhnRmUHTa5skHNDkO-fHharfMx-MmoKeb33wuaK-NczLvg-9zZ0Y_e7SMqtcVgtSnsoGdldG6HzmHf4-TDPjW7OZVpG_y82ebzWASzSQLTQay3Kvinh2XRXmfvOnTR3JzqVfZy9_X59r5YP35b3S7XhaoJmwrQHaVEUwqKG6i50kzyhrRalhWXyLXsEFRTk5I2rNSStrQG06BhgLKkbXmVrY682uNOjMH2GPbCoxX_Bj5sBIbJKmdETZM7nCMzlFRNKbmRkrKWpzl0SKrE9enIlUz6NZs4iZ2fw5CeL2iZULylLUuo-ohKX40xmO6sCkQcchSvOYpDjuKUY9r7eGKfZW_0ees1tQT4cgQkv33o8bcPTosJ986HLmCKMybwfzX-Al7Wq_4</recordid><startdate>201912</startdate><enddate>201912</enddate><creator>Deng, Wenyan</creator><creator>Chen, Kai</creator><creator>Liu, Shuxia</creator><creator>Wang, Yingying</creator><general>Taylor & Francis</general><general>Taylor & Francis Ltd</general><general>Taylor & Francis Group</general><scope>0YH</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>DOA</scope><orcidid>https://orcid.org/0000-0002-3457-5393</orcidid></search><sort><creationdate>201912</creationdate><title>Silencing circular ANRIL protects HK-2 cells from lipopolysaccharide-induced inflammatory injury through up-regulating microRNA-9</title><author>Deng, Wenyan ; Chen, Kai ; Liu, Shuxia ; Wang, Yingying</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c507t-1df220d221c8e158cd7b8609db348ba8dbfa1c65032673db29251e6ae71ab3293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Antisense RNA</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cell viability</topic><topic>Chronic kidney disease</topic><topic>circular ANRIL</topic><topic>Cyclin-dependent kinase inhibitors</topic><topic>Cytokines</topic><topic>Endothelial cells</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Gene Silencing</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - genetics</topic><topic>Inflammation - pathology</topic><topic>Inflammatory response</topic><topic>Injuries</topic><topic>INK4 protein</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>Kidney diseases</topic><topic>lipopolysaccharide</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>microRNA-9</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>miRNA</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Non-coding RNA</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - genetics</topic><topic>Transfection</topic><topic>Up-Regulation - drug effects</topic><topic>Up-Regulation - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Deng, Wenyan</creatorcontrib><creatorcontrib>Chen, Kai</creatorcontrib><creatorcontrib>Liu, Shuxia</creatorcontrib><creatorcontrib>Wang, Yingying</creatorcontrib><collection>Taylor & Francis 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>DOAJ Directory of Open Access Journals</collection><jtitle>Artificial cells, nanomedicine, and biotechnology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Deng, Wenyan</au><au>Chen, Kai</au><au>Liu, Shuxia</au><au>Wang, Yingying</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Silencing circular ANRIL protects HK-2 cells from lipopolysaccharide-induced inflammatory injury through up-regulating microRNA-9</atitle><jtitle>Artificial cells, nanomedicine, and biotechnology</jtitle><addtitle>Artif Cells Nanomed Biotechnol</addtitle><date>2019-12</date><risdate>2019</risdate><volume>47</volume><issue>1</issue><spage>3478</spage><epage>3484</epage><pages>3478-3484</pages><issn>2169-1401</issn><eissn>2169-141X</eissn><abstract>Circular antisense non-coding RNA in the INK4 locus (cANRIL) participated in inflammation of endothelial cells. However, whether cANRIL is associated with inflammatory injury of HK-2 cells, thereby affecting chronic kidney disease has not been investigated. We tested the hypothesis that cANRIL participated in inflammatory response in vitro. HK-2 cells were stimulated by lipopolysaccharides (LPS). RT-qPCR was executed for cANRIL expression assessment. After transfection, cell viability, apoptosis, inflammatory cytokines and ROS generation were appraised to evaluate the impact of silencing cANRIL on LPS-induced inflammatory injury. The regulatory relationship between cANRIL and microRNA-9 (miR-9) was verified. In addition, whether miR-9 affected LPS-induced inflammatory injury was measured after miR-9 inhibitor transfection. Western blot was utilized to detect NF-κB and JNK/p38 pathway-related proteins. The results showed that LPS promoted cANRIL expression and cell injuries in HK-2 cells. Furthermore, silencing cANRIL alleviated inflammatory injuries by promoting viability, suppressing apoptosis, inflammatory cytokines and ROS generation in HK-2 cells. In addition, miR-9 expression was accelerated by silencing cANRIL. Meanwhile, miR-9 down-regulation invalidated the effect of silencing cANRIL on inflammation and NF-κB and JNK/p38 pathways. The study clarified that silencing cANRIL hindered NF-κB and JNK/p38 pathways by positively regulating miR-9, thereby protecting HK-2 cells from LPS-induced injury.</abstract><cop>England</cop><pub>Taylor & Francis</pub><pmid>31432701</pmid><doi>10.1080/21691401.2019.1652187</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0002-3457-5393</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Antisense RNA Apoptosis Apoptosis - drug effects Apoptosis - genetics Cell Line, Tumor Cell viability Chronic kidney disease circular ANRIL Cyclin-dependent kinase inhibitors Cytokines Endothelial cells Gene Expression Regulation, Neoplastic - drug effects Gene Expression Regulation, Neoplastic - genetics Gene Silencing Humans Inflammation Inflammation - chemically induced Inflammation - genetics Inflammation - pathology Inflammatory response Injuries INK4 protein JNK Mitogen-Activated Protein Kinases - metabolism Kidney diseases lipopolysaccharide Lipopolysaccharides Lipopolysaccharides - pharmacology microRNA-9 MicroRNAs MicroRNAs - genetics miRNA NF-kappa B - metabolism NF-κB protein Non-coding RNA p38 Mitogen-Activated Protein Kinases - metabolism Ribonucleic acid RNA RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Signal Transduction - drug effects Signal Transduction - genetics Transfection Up-Regulation - drug effects Up-Regulation - genetics |
| title | Silencing circular ANRIL protects HK-2 cells from lipopolysaccharide-induced inflammatory injury through up-regulating microRNA-9 |
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