MicroRNA-206 promotes lipopolysaccharide-induced inflammation injury via regulation of IRAK1 in MRC-5 cells
MicroRNAs (miRNAs) have been reported to play crucial role in the airway inflammatory diseases. However, the involvement of miR-206 in airway inflammatory diseases is still uninvestigated. The study aimed to explore the effect of miR-206 on lipopolysaccharide (LPS)-induced inflammation injury in MRC...
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| Veröffentlicht in: | International immunopharmacology 2019-08, Vol.73, p.590-598 |
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| creator | Chu, Heying Qu, Xiangwen Wang, Feng Chang, Jingxia Cheng, Ruirui Song, Xiangjin Chen, Tengfei Zhang, Guojun |
| description | MicroRNAs (miRNAs) have been reported to play crucial role in the airway inflammatory diseases. However, the involvement of miR-206 in airway inflammatory diseases is still uninvestigated. The study aimed to explore the effect of miR-206 on lipopolysaccharide (LPS)-induced inflammation injury in MRC-5 cells, and point out a potential relevance for chronic obstructive pulmonary disease (COPD).
LPS was utilized to expose MRC-5 cells, then cell viability, cell migration, apoptosis, apoptosis-associated factors, as well as the concentrations and protein levels of IL-6 and IL-8 were explored. After transfected with miR-206 mimic and inhibitor, above parameters were reassessed in LPS-injured cells. Expression level of IRAK1 was examined in miR-206 mimic/inhibitor transfected cells by using RT-qPCR. The effect of IRAK1 on LPS-induced inflammation injury was investigated in MRC-5 cells after transfection with pc-IRAK1 and sh-IRAK1. The effects of miR-206 and IRAK1 on MEK/ERK and JNK pathways were determined by western blot assay.
LPS significantly triggered inflammation injury in MRC-5 cells by inhibiting cell viability, suppressing the healing of scratches, inducing cell apoptosis, down-regulating Bcl-2 expression and up-regulating Bax, cleaved-Caspase-3 and cleaved-Caspase-9 expression, and concurrently increasing the concentrations and the protein levels of IL-6 and IL-8. MiR-206 overexpression aggravated LPS-induced inflammation injury in MRC-5 cells. Up-regulation of IRAK1 was observed in miR-206 mimic-transfected cells. Moreover, IRAK1 overexpression promoted LPS-induced inflammation injury in MRC-5 cells. MiR-206 activated MEK/ERK and JNK pathways by regulating IRAK1.
MiR-206 promotes LPS-induced inflammation injury through regulation of IRAK1 in MRC-5 cells.
•LPS induces inflammation injury in MRC-5 cells.•MiR-206 promotes LPS-induced inflammation injury in MRC-5 cells.•MiR-206 up-regulates IRAK1 expression in MRC-5 cells.•IRAK1 promotes LPS-induced inflammation injury in MRC-5 cells.•MiR-206 activates MEK/ERK and JNK pathways via regulating IRAK1. |
| doi_str_mv | 10.1016/j.intimp.2019.05.029 |
| format | Article |
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LPS was utilized to expose MRC-5 cells, then cell viability, cell migration, apoptosis, apoptosis-associated factors, as well as the concentrations and protein levels of IL-6 and IL-8 were explored. After transfected with miR-206 mimic and inhibitor, above parameters were reassessed in LPS-injured cells. Expression level of IRAK1 was examined in miR-206 mimic/inhibitor transfected cells by using RT-qPCR. The effect of IRAK1 on LPS-induced inflammation injury was investigated in MRC-5 cells after transfection with pc-IRAK1 and sh-IRAK1. The effects of miR-206 and IRAK1 on MEK/ERK and JNK pathways were determined by western blot assay.
LPS significantly triggered inflammation injury in MRC-5 cells by inhibiting cell viability, suppressing the healing of scratches, inducing cell apoptosis, down-regulating Bcl-2 expression and up-regulating Bax, cleaved-Caspase-3 and cleaved-Caspase-9 expression, and concurrently increasing the concentrations and the protein levels of IL-6 and IL-8. MiR-206 overexpression aggravated LPS-induced inflammation injury in MRC-5 cells. Up-regulation of IRAK1 was observed in miR-206 mimic-transfected cells. Moreover, IRAK1 overexpression promoted LPS-induced inflammation injury in MRC-5 cells. MiR-206 activated MEK/ERK and JNK pathways by regulating IRAK1.
MiR-206 promotes LPS-induced inflammation injury through regulation of IRAK1 in MRC-5 cells.
•LPS induces inflammation injury in MRC-5 cells.•MiR-206 promotes LPS-induced inflammation injury in MRC-5 cells.•MiR-206 up-regulates IRAK1 expression in MRC-5 cells.•IRAK1 promotes LPS-induced inflammation injury in MRC-5 cells.•MiR-206 activates MEK/ERK and JNK pathways via regulating IRAK1.</description><identifier>ISSN: 1567-5769</identifier><identifier>EISSN: 1878-1705</identifier><identifier>DOI: 10.1016/j.intimp.2019.05.029</identifier><identifier>PMID: 31279225</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Apoptosis ; BAX protein ; Bcl-2 protein ; Caspase ; Caspase-3 ; Caspase-9 ; Cell adhesion & migration ; Cell Line ; Cell migration ; Cell viability ; Chronic obstructive pulmonary disease ; Chronic obstructive pulmonary disease (COPD) ; Humans ; Inflammation ; Inflammation - metabolism ; Inflammatory diseases ; Inhibitors ; Injuries ; Interleukin 6 ; Interleukin 8 ; Interleukin-1 Receptor-Associated Kinases - genetics ; Interleukin-1 Receptor-Associated Kinases - metabolism ; Interleukin-6 - metabolism ; Interleukin-8 - metabolism ; IRAK protein ; IRAK1 ; JNK ; Levels ; Lipopolysaccharide ; Lipopolysaccharides ; Lung diseases ; MAP Kinase Signaling System - drug effects ; MEK/ERK ; microRNA-206 ; MicroRNAs ; MicroRNAs - metabolism ; miRNA ; Obstructive lung disease ; Proteins ; Respiratory tract ; Respiratory tract diseases ; Ribonucleic acid ; RNA ; Transfection</subject><ispartof>International immunopharmacology, 2019-08, Vol.73, p.590-598</ispartof><rights>2019</rights><rights>Copyright © 2019. Published by Elsevier B.V.</rights><rights>Copyright Elsevier BV Aug 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-7ad9e7af3761d4504a01236273b6cecc6ff12da4bafeca837a7b6d9f290610823</citedby><cites>FETCH-LOGICAL-c390t-7ad9e7af3761d4504a01236273b6cecc6ff12da4bafeca837a7b6d9f290610823</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1567576918314474$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31279225$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chu, Heying</creatorcontrib><creatorcontrib>Qu, Xiangwen</creatorcontrib><creatorcontrib>Wang, Feng</creatorcontrib><creatorcontrib>Chang, Jingxia</creatorcontrib><creatorcontrib>Cheng, Ruirui</creatorcontrib><creatorcontrib>Song, Xiangjin</creatorcontrib><creatorcontrib>Chen, Tengfei</creatorcontrib><creatorcontrib>Zhang, Guojun</creatorcontrib><title>MicroRNA-206 promotes lipopolysaccharide-induced inflammation injury via regulation of IRAK1 in MRC-5 cells</title><title>International immunopharmacology</title><addtitle>Int Immunopharmacol</addtitle><description>MicroRNAs (miRNAs) have been reported to play crucial role in the airway inflammatory diseases. However, the involvement of miR-206 in airway inflammatory diseases is still uninvestigated. The study aimed to explore the effect of miR-206 on lipopolysaccharide (LPS)-induced inflammation injury in MRC-5 cells, and point out a potential relevance for chronic obstructive pulmonary disease (COPD).
LPS was utilized to expose MRC-5 cells, then cell viability, cell migration, apoptosis, apoptosis-associated factors, as well as the concentrations and protein levels of IL-6 and IL-8 were explored. After transfected with miR-206 mimic and inhibitor, above parameters were reassessed in LPS-injured cells. Expression level of IRAK1 was examined in miR-206 mimic/inhibitor transfected cells by using RT-qPCR. The effect of IRAK1 on LPS-induced inflammation injury was investigated in MRC-5 cells after transfection with pc-IRAK1 and sh-IRAK1. The effects of miR-206 and IRAK1 on MEK/ERK and JNK pathways were determined by western blot assay.
LPS significantly triggered inflammation injury in MRC-5 cells by inhibiting cell viability, suppressing the healing of scratches, inducing cell apoptosis, down-regulating Bcl-2 expression and up-regulating Bax, cleaved-Caspase-3 and cleaved-Caspase-9 expression, and concurrently increasing the concentrations and the protein levels of IL-6 and IL-8. MiR-206 overexpression aggravated LPS-induced inflammation injury in MRC-5 cells. Up-regulation of IRAK1 was observed in miR-206 mimic-transfected cells. Moreover, IRAK1 overexpression promoted LPS-induced inflammation injury in MRC-5 cells. MiR-206 activated MEK/ERK and JNK pathways by regulating IRAK1.
MiR-206 promotes LPS-induced inflammation injury through regulation of IRAK1 in MRC-5 cells.
•LPS induces inflammation injury in MRC-5 cells.•MiR-206 promotes LPS-induced inflammation injury in MRC-5 cells.•MiR-206 up-regulates IRAK1 expression in MRC-5 cells.•IRAK1 promotes LPS-induced inflammation injury in MRC-5 cells.•MiR-206 activates MEK/ERK and JNK pathways via regulating IRAK1.</description><subject>Apoptosis</subject><subject>BAX protein</subject><subject>Bcl-2 protein</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Caspase-9</subject><subject>Cell adhesion & migration</subject><subject>Cell Line</subject><subject>Cell migration</subject><subject>Cell viability</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Chronic obstructive pulmonary disease (COPD)</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - metabolism</subject><subject>Inflammatory diseases</subject><subject>Inhibitors</subject><subject>Injuries</subject><subject>Interleukin 6</subject><subject>Interleukin 8</subject><subject>Interleukin-1 Receptor-Associated Kinases - genetics</subject><subject>Interleukin-1 Receptor-Associated Kinases - metabolism</subject><subject>Interleukin-6 - metabolism</subject><subject>Interleukin-8 - metabolism</subject><subject>IRAK protein</subject><subject>IRAK1</subject><subject>JNK</subject><subject>Levels</subject><subject>Lipopolysaccharide</subject><subject>Lipopolysaccharides</subject><subject>Lung diseases</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>MEK/ERK</subject><subject>microRNA-206</subject><subject>MicroRNAs</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Obstructive lung disease</subject><subject>Proteins</subject><subject>Respiratory tract</subject><subject>Respiratory tract diseases</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Transfection</subject><issn>1567-5769</issn><issn>1878-1705</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU2P1SAUhonROOPoPzCmiRs3rQdaoN2Y3NyMOnFGkxtdEy4clNqWCu0k99_LTUcXLlwBh-d8vS8hLylUFKh421d-Wvw4VwxoVwGvgHWPyCVtZVtSCfxxvnMhSy5Fd0GepdQD5HhDn5KLmjLZMcYvyc87b2I4fN6VDEQxxzCGBVMx-DnMYTglbcwPHb3F0k92NWgLP7lBj6NefJjyo1_jqbj3uoj4fR22aHDFzWH3iebv4u6wL3lhcBjSc_LE6SHhi4fzinx7f_11_7G8_fLhZr-7LU3dwVJKbTuU2tVSUNtwaDRQVgsm66MwaIxwjjKrm6N2aHRbSy2PwnaOdSAotKy-Im-2unmdXyumRY0-nSfQE4Y1qbx4zdpWgszo63_QPqxxytNlSkjZ8JafCzYblaVKKaJTc_SjjidFQZ3NUL3azFBnMxRwlc3Iaa8eiq_HEe3fpD_qZ-DdBmBW495jVMl4nLLKPqJZlA3-_x1-A1MRnC8</recordid><startdate>201908</startdate><enddate>201908</enddate><creator>Chu, Heying</creator><creator>Qu, Xiangwen</creator><creator>Wang, Feng</creator><creator>Chang, Jingxia</creator><creator>Cheng, Ruirui</creator><creator>Song, Xiangjin</creator><creator>Chen, Tengfei</creator><creator>Zhang, Guojun</creator><general>Elsevier B.V</general><general>Elsevier BV</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>7QO</scope><scope>7T5</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201908</creationdate><title>MicroRNA-206 promotes lipopolysaccharide-induced inflammation injury via regulation of IRAK1 in MRC-5 cells</title><author>Chu, Heying ; Qu, Xiangwen ; Wang, Feng ; Chang, Jingxia ; Cheng, Ruirui ; Song, Xiangjin ; Chen, Tengfei ; Zhang, Guojun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-7ad9e7af3761d4504a01236273b6cecc6ff12da4bafeca837a7b6d9f290610823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Apoptosis</topic><topic>BAX protein</topic><topic>Bcl-2 protein</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>Caspase-9</topic><topic>Cell adhesion & migration</topic><topic>Cell Line</topic><topic>Cell migration</topic><topic>Cell viability</topic><topic>Chronic obstructive pulmonary disease</topic><topic>Chronic obstructive pulmonary disease (COPD)</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation - metabolism</topic><topic>Inflammatory diseases</topic><topic>Inhibitors</topic><topic>Injuries</topic><topic>Interleukin 6</topic><topic>Interleukin 8</topic><topic>Interleukin-1 Receptor-Associated Kinases - genetics</topic><topic>Interleukin-1 Receptor-Associated Kinases - metabolism</topic><topic>Interleukin-6 - metabolism</topic><topic>Interleukin-8 - metabolism</topic><topic>IRAK protein</topic><topic>IRAK1</topic><topic>JNK</topic><topic>Levels</topic><topic>Lipopolysaccharide</topic><topic>Lipopolysaccharides</topic><topic>Lung diseases</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>MEK/ERK</topic><topic>microRNA-206</topic><topic>MicroRNAs</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Obstructive lung disease</topic><topic>Proteins</topic><topic>Respiratory tract</topic><topic>Respiratory tract diseases</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chu, Heying</creatorcontrib><creatorcontrib>Qu, Xiangwen</creatorcontrib><creatorcontrib>Wang, Feng</creatorcontrib><creatorcontrib>Chang, Jingxia</creatorcontrib><creatorcontrib>Cheng, Ruirui</creatorcontrib><creatorcontrib>Song, Xiangjin</creatorcontrib><creatorcontrib>Chen, Tengfei</creatorcontrib><creatorcontrib>Zhang, Guojun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chu, Heying</au><au>Qu, Xiangwen</au><au>Wang, Feng</au><au>Chang, Jingxia</au><au>Cheng, Ruirui</au><au>Song, Xiangjin</au><au>Chen, Tengfei</au><au>Zhang, Guojun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA-206 promotes lipopolysaccharide-induced inflammation injury via regulation of IRAK1 in MRC-5 cells</atitle><jtitle>International immunopharmacology</jtitle><addtitle>Int Immunopharmacol</addtitle><date>2019-08</date><risdate>2019</risdate><volume>73</volume><spage>590</spage><epage>598</epage><pages>590-598</pages><issn>1567-5769</issn><eissn>1878-1705</eissn><abstract>MicroRNAs (miRNAs) have been reported to play crucial role in the airway inflammatory diseases. However, the involvement of miR-206 in airway inflammatory diseases is still uninvestigated. The study aimed to explore the effect of miR-206 on lipopolysaccharide (LPS)-induced inflammation injury in MRC-5 cells, and point out a potential relevance for chronic obstructive pulmonary disease (COPD).
LPS was utilized to expose MRC-5 cells, then cell viability, cell migration, apoptosis, apoptosis-associated factors, as well as the concentrations and protein levels of IL-6 and IL-8 were explored. After transfected with miR-206 mimic and inhibitor, above parameters were reassessed in LPS-injured cells. Expression level of IRAK1 was examined in miR-206 mimic/inhibitor transfected cells by using RT-qPCR. The effect of IRAK1 on LPS-induced inflammation injury was investigated in MRC-5 cells after transfection with pc-IRAK1 and sh-IRAK1. The effects of miR-206 and IRAK1 on MEK/ERK and JNK pathways were determined by western blot assay.
LPS significantly triggered inflammation injury in MRC-5 cells by inhibiting cell viability, suppressing the healing of scratches, inducing cell apoptosis, down-regulating Bcl-2 expression and up-regulating Bax, cleaved-Caspase-3 and cleaved-Caspase-9 expression, and concurrently increasing the concentrations and the protein levels of IL-6 and IL-8. MiR-206 overexpression aggravated LPS-induced inflammation injury in MRC-5 cells. Up-regulation of IRAK1 was observed in miR-206 mimic-transfected cells. Moreover, IRAK1 overexpression promoted LPS-induced inflammation injury in MRC-5 cells. MiR-206 activated MEK/ERK and JNK pathways by regulating IRAK1.
MiR-206 promotes LPS-induced inflammation injury through regulation of IRAK1 in MRC-5 cells.
•LPS induces inflammation injury in MRC-5 cells.•MiR-206 promotes LPS-induced inflammation injury in MRC-5 cells.•MiR-206 up-regulates IRAK1 expression in MRC-5 cells.•IRAK1 promotes LPS-induced inflammation injury in MRC-5 cells.•MiR-206 activates MEK/ERK and JNK pathways via regulating IRAK1.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>31279225</pmid><doi>10.1016/j.intimp.2019.05.029</doi><tpages>9</tpages></addata></record> |
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| subjects | Apoptosis BAX protein Bcl-2 protein Caspase Caspase-3 Caspase-9 Cell adhesion & migration Cell Line Cell migration Cell viability Chronic obstructive pulmonary disease Chronic obstructive pulmonary disease (COPD) Humans Inflammation Inflammation - metabolism Inflammatory diseases Inhibitors Injuries Interleukin 6 Interleukin 8 Interleukin-1 Receptor-Associated Kinases - genetics Interleukin-1 Receptor-Associated Kinases - metabolism Interleukin-6 - metabolism Interleukin-8 - metabolism IRAK protein IRAK1 JNK Levels Lipopolysaccharide Lipopolysaccharides Lung diseases MAP Kinase Signaling System - drug effects MEK/ERK microRNA-206 MicroRNAs MicroRNAs - metabolism miRNA Obstructive lung disease Proteins Respiratory tract Respiratory tract diseases Ribonucleic acid RNA Transfection |
| title | MicroRNA-206 promotes lipopolysaccharide-induced inflammation injury via regulation of IRAK1 in MRC-5 cells |
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