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RAGE/NF-κB Pathway Mediates Lipopolysaccharide-Induced Inflammation in Alveolar Type I Epithelial Cells Isolated from Neonate Rats
Alveolar type I epithelial cells (AECIs) play an important role in the pathogenesis of acute lung injury. The receptor for advanced glycation end-products (RAGEs) is expressed at a high basal level in AECIs, and its soluble isoform is suggested as a marker of AECI injury. However, the molecular mech...
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| Published in: | Inflammation 2014-10, Vol.37 (5), p.1623-1629 |
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| container_end_page | 1629 |
| container_issue | 5 |
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| container_title | Inflammation |
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| creator | Li, Yuhong Wu, Rong Zhao, Sai Cheng, Huaipin Ji, Ping Yu, Min Tian, Zhaofang |
| description | Alveolar type I epithelial cells (AECIs) play an important role in the pathogenesis of acute lung injury. The receptor for advanced glycation end-products (RAGEs) is expressed at a high basal level in AECIs, and its soluble isoform is suggested as a marker of AECI injury. However, the molecular mechanism by which RAGE mediates inflammatory injury in AECIs remains elusive. In this study, we established lipopolysaccharide (LPS)-induced inflammation in AECIs isolated from neonate rats as the experimental model and investigated the role of RAGE/NF-κB signaling in mediating inflammatory response in AECIs. We found that LPS increased RAGE expression and the secretion of tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) in AECIs in a dose-dependent manner. Knockdown of RAGE significantly decreased TNF-α and IL-1β levels in conditioned medium of AECIs. Electrophoretic mobility shift assay (EMSA) showed that NF-κB activation was increased in AECIs treated by LPS. However, knockdown of RAGE inhibited both basic and LPS-induced NF-κB activity in AECIs. Finally, NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) significantly reduced LPS-induced upregulation of RAGE expression at both protein and messenger RNA (mRNA) levels in AECIs. Our results suggest that RAGE mediates inflammatory response in AECIs via activating NF-κB, and RAGE/NF-κB pathway presents potential target for the prevention and therapy of acute lung injury. |
| doi_str_mv | 10.1007/s10753-014-9889-y |
| format | article |
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The receptor for advanced glycation end-products (RAGEs) is expressed at a high basal level in AECIs, and its soluble isoform is suggested as a marker of AECI injury. However, the molecular mechanism by which RAGE mediates inflammatory injury in AECIs remains elusive. In this study, we established lipopolysaccharide (LPS)-induced inflammation in AECIs isolated from neonate rats as the experimental model and investigated the role of RAGE/NF-κB signaling in mediating inflammatory response in AECIs. We found that LPS increased RAGE expression and the secretion of tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) in AECIs in a dose-dependent manner. Knockdown of RAGE significantly decreased TNF-α and IL-1β levels in conditioned medium of AECIs. Electrophoretic mobility shift assay (EMSA) showed that NF-κB activation was increased in AECIs treated by LPS. However, knockdown of RAGE inhibited both basic and LPS-induced NF-κB activity in AECIs. Finally, NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) significantly reduced LPS-induced upregulation of RAGE expression at both protein and messenger RNA (mRNA) levels in AECIs. Our results suggest that RAGE mediates inflammatory response in AECIs via activating NF-κB, and RAGE/NF-κB pathway presents potential target for the prevention and therapy of acute lung injury.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-014-9889-y</identifier><identifier>PMID: 24740410</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Animals ; Animals, Newborn ; Biomedical and Life Sciences ; Biomedicine ; Immunology ; Inflammation - chemically induced ; Inflammation - metabolism ; Internal Medicine ; Lipopolysaccharides - toxicity ; Lung - drug effects ; Lung - metabolism ; NF-kappa B - biosynthesis ; Pathology ; Pharmacology/Toxicology ; Pulmonary Alveoli - drug effects ; Pulmonary Alveoli - metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor for Advanced Glycation End Products ; Receptors, Immunologic - biosynthesis ; Respiratory Mucosa - drug effects ; Respiratory Mucosa - metabolism ; Rheumatology</subject><ispartof>Inflammation, 2014-10, Vol.37 (5), p.1623-1629</ispartof><rights>Springer Science+Business Media New York 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-6698a13f984c6a4d3dbe44f2afb3e71febb86727cc50e49e6cdc6afdc96b7eac3</citedby><cites>FETCH-LOGICAL-c447t-6698a13f984c6a4d3dbe44f2afb3e71febb86727cc50e49e6cdc6afdc96b7eac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24740410$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Yuhong</creatorcontrib><creatorcontrib>Wu, Rong</creatorcontrib><creatorcontrib>Zhao, Sai</creatorcontrib><creatorcontrib>Cheng, Huaipin</creatorcontrib><creatorcontrib>Ji, Ping</creatorcontrib><creatorcontrib>Yu, Min</creatorcontrib><creatorcontrib>Tian, Zhaofang</creatorcontrib><title>RAGE/NF-κB Pathway Mediates Lipopolysaccharide-Induced Inflammation in Alveolar Type I Epithelial Cells Isolated from Neonate Rats</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>Alveolar type I epithelial cells (AECIs) play an important role in the pathogenesis of acute lung injury. The receptor for advanced glycation end-products (RAGEs) is expressed at a high basal level in AECIs, and its soluble isoform is suggested as a marker of AECI injury. However, the molecular mechanism by which RAGE mediates inflammatory injury in AECIs remains elusive. In this study, we established lipopolysaccharide (LPS)-induced inflammation in AECIs isolated from neonate rats as the experimental model and investigated the role of RAGE/NF-κB signaling in mediating inflammatory response in AECIs. We found that LPS increased RAGE expression and the secretion of tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) in AECIs in a dose-dependent manner. Knockdown of RAGE significantly decreased TNF-α and IL-1β levels in conditioned medium of AECIs. Electrophoretic mobility shift assay (EMSA) showed that NF-κB activation was increased in AECIs treated by LPS. However, knockdown of RAGE inhibited both basic and LPS-induced NF-κB activity in AECIs. Finally, NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) significantly reduced LPS-induced upregulation of RAGE expression at both protein and messenger RNA (mRNA) levels in AECIs. Our results suggest that RAGE mediates inflammatory response in AECIs via activating NF-κB, and RAGE/NF-κB pathway presents potential target for the prevention and therapy of acute lung injury.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Immunology</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - metabolism</subject><subject>Internal Medicine</subject><subject>Lipopolysaccharides - toxicity</subject><subject>Lung - drug effects</subject><subject>Lung - metabolism</subject><subject>NF-kappa B - biosynthesis</subject><subject>Pathology</subject><subject>Pharmacology/Toxicology</subject><subject>Pulmonary Alveoli - drug effects</subject><subject>Pulmonary Alveoli - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor for Advanced Glycation End Products</subject><subject>Receptors, Immunologic - biosynthesis</subject><subject>Respiratory Mucosa - drug effects</subject><subject>Respiratory Mucosa - metabolism</subject><subject>Rheumatology</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><recordid>eNp9kMFu1DAURS1ERaeFD2CDvGTj1o49drwcRtM20tCiqqwtx3lhXCVxsBNQ1v0rPoJvwtUUlqyerHfu1fNB6D2jF4xSdZkYVWtOKBNEl6Umyyu0YmvFSbFW8jVaUS4p4VqrU3SW0iOltNQlf4NOC6EEFYyu0NP95np3eXtFfv_6hL_Y6fDTLvgzNN5OkPDej2EM3ZKscwcbfQOkGprZQYOroe1s39vJhwH7AW-6HxA6G_HDMgKu8G700wE6bzu8ha5LuEp5PeVkG0OPbyEM-YXv7ZTeopPWdgnevcxz9PVq97C9Ifu762q72RMnhJqIlLq0jLe6FE5a0fCmBiHawrY1B8VaqOtSqkI5t6YgNEjXZK5tnJa1Auv4Ofp47B1j-D5Dmkzvk8vH2QHCnAyTjMmCUc0zyo6oiyGlCK0Zo-9tXAyj5tm9Obo32b15dm-WnPnwUj_XPTT_En9lZ6A4Aimvhm8QzWOY45C__J_WP4HmkqE</recordid><startdate>20141001</startdate><enddate>20141001</enddate><creator>Li, Yuhong</creator><creator>Wu, Rong</creator><creator>Zhao, Sai</creator><creator>Cheng, Huaipin</creator><creator>Ji, Ping</creator><creator>Yu, Min</creator><creator>Tian, Zhaofang</creator><general>Springer US</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>7T5</scope><scope>H94</scope></search><sort><creationdate>20141001</creationdate><title>RAGE/NF-κB Pathway Mediates Lipopolysaccharide-Induced Inflammation in Alveolar Type I Epithelial Cells Isolated from Neonate Rats</title><author>Li, Yuhong ; Wu, Rong ; Zhao, Sai ; Cheng, Huaipin ; Ji, Ping ; Yu, Min ; Tian, Zhaofang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-6698a13f984c6a4d3dbe44f2afb3e71febb86727cc50e49e6cdc6afdc96b7eac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Immunology</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - metabolism</topic><topic>Internal Medicine</topic><topic>Lipopolysaccharides - toxicity</topic><topic>Lung - drug effects</topic><topic>Lung - metabolism</topic><topic>NF-kappa B - biosynthesis</topic><topic>Pathology</topic><topic>Pharmacology/Toxicology</topic><topic>Pulmonary Alveoli - drug effects</topic><topic>Pulmonary Alveoli - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor for Advanced Glycation End Products</topic><topic>Receptors, Immunologic - biosynthesis</topic><topic>Respiratory Mucosa - drug effects</topic><topic>Respiratory Mucosa - metabolism</topic><topic>Rheumatology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Yuhong</creatorcontrib><creatorcontrib>Wu, Rong</creatorcontrib><creatorcontrib>Zhao, Sai</creatorcontrib><creatorcontrib>Cheng, Huaipin</creatorcontrib><creatorcontrib>Ji, Ping</creatorcontrib><creatorcontrib>Yu, Min</creatorcontrib><creatorcontrib>Tian, Zhaofang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Yuhong</au><au>Wu, Rong</au><au>Zhao, Sai</au><au>Cheng, Huaipin</au><au>Ji, Ping</au><au>Yu, Min</au><au>Tian, Zhaofang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>RAGE/NF-κB Pathway Mediates Lipopolysaccharide-Induced Inflammation in Alveolar Type I Epithelial Cells Isolated from Neonate Rats</atitle><jtitle>Inflammation</jtitle><stitle>Inflammation</stitle><addtitle>Inflammation</addtitle><date>2014-10-01</date><risdate>2014</risdate><volume>37</volume><issue>5</issue><spage>1623</spage><epage>1629</epage><pages>1623-1629</pages><issn>0360-3997</issn><eissn>1573-2576</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Alveolar type I epithelial cells (AECIs) play an important role in the pathogenesis of acute lung injury. The receptor for advanced glycation end-products (RAGEs) is expressed at a high basal level in AECIs, and its soluble isoform is suggested as a marker of AECI injury. However, the molecular mechanism by which RAGE mediates inflammatory injury in AECIs remains elusive. In this study, we established lipopolysaccharide (LPS)-induced inflammation in AECIs isolated from neonate rats as the experimental model and investigated the role of RAGE/NF-κB signaling in mediating inflammatory response in AECIs. We found that LPS increased RAGE expression and the secretion of tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) in AECIs in a dose-dependent manner. Knockdown of RAGE significantly decreased TNF-α and IL-1β levels in conditioned medium of AECIs. Electrophoretic mobility shift assay (EMSA) showed that NF-κB activation was increased in AECIs treated by LPS. However, knockdown of RAGE inhibited both basic and LPS-induced NF-κB activity in AECIs. Finally, NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) significantly reduced LPS-induced upregulation of RAGE expression at both protein and messenger RNA (mRNA) levels in AECIs. Our results suggest that RAGE mediates inflammatory response in AECIs via activating NF-κB, and RAGE/NF-κB pathway presents potential target for the prevention and therapy of acute lung injury.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>24740410</pmid><doi>10.1007/s10753-014-9889-y</doi><tpages>7</tpages></addata></record> |
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| subjects | Animals Animals, Newborn Biomedical and Life Sciences Biomedicine Immunology Inflammation - chemically induced Inflammation - metabolism Internal Medicine Lipopolysaccharides - toxicity Lung - drug effects Lung - metabolism NF-kappa B - biosynthesis Pathology Pharmacology/Toxicology Pulmonary Alveoli - drug effects Pulmonary Alveoli - metabolism Rats Rats, Sprague-Dawley Receptor for Advanced Glycation End Products Receptors, Immunologic - biosynthesis Respiratory Mucosa - drug effects Respiratory Mucosa - metabolism Rheumatology |
| title | RAGE/NF-κB Pathway Mediates Lipopolysaccharide-Induced Inflammation in Alveolar Type I Epithelial Cells Isolated from Neonate Rats |
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