Lipopolysaccharide induces VCAM-1 expression and neutrophil adhesion to human tracheal smooth muscle cells: Involvement of Src/EGFR/PI3-K/Akt pathway
In our previous study, LPS has been shown to induce vascular cell adhesion molecule-1(VCAM-1) expression through MAPKs and NF-κB in human tracheal smooth muscle cells (HTSMCs). In addition to these pathways, the non-receptor tyrosine kinases (Src), EGF receptor (EGFR), and phosphatidylinositol 3-kin...
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description | In our previous study, LPS has been shown to induce vascular cell adhesion molecule-1(VCAM-1) expression through MAPKs and NF-κB in human tracheal smooth muscle cells (HTSMCs). In addition to these pathways, the non-receptor tyrosine kinases (Src), EGF receptor (EGFR), and phosphatidylinositol 3-kinase (PI3K) have been shown to be implicated in the expression of several inflammatory target proteins. Here, we reported that LPS-induced up-regulation of VCAM-1 enhanced the adhesion of neutrophils onto HTSMC monolayer, which was inhibited by LY294002 and wortmannin. LPS stimulated phosphorylation of protein tyrosine kinases including Src, PYK2, and EGFR, which were further confirmed using specific anti-phospho-Src, PYK2, or EGFR Ab, respectively, revealed by Western blotting. LPS-stimulated Src, PYK2, EGFR, and Akt phosphorylation and VCAM-1 expression were attenuated by the inhibitors of Src (PP1), EGFR (AG1478), PI3-K (LY294002 and wortmannin), and Akt (SH-5), respectively, or transfection with siRNAs of Src or Akt and shRNA of p110. LPS-induced VCAM-1 expression was also blocked by pretreatment with curcumin (a p300 inhibitor) or transfection with p300 siRNA. LPS-stimulated Akt activation translocated into nucleus and associated with p300 and VCAM-1 promoter region was further confirmed by immunofluorescence, immunoprecipitation, and chromatin immunoprecipitation assays. This association of Akt and p300 to VCAM-1 promoter was inhibited by pretreatment with PP1, AG1478, wortmannin, and SH-5. LPS-induced p300 activation enhanced VCAM-1 promoter activity and VCAM-1 mRNA expression. These results suggested that in HTSMCs, Akt phosphorylation mediated through transactivation of Src/PYK2/EGFR promoted the transcriptional p300 activity and eventually led to VCAM-1 expression induced by LPS. |
doi_str_mv | 10.1016/j.taap.2007.11.026 |
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In addition to these pathways, the non-receptor tyrosine kinases (Src), EGF receptor (EGFR), and phosphatidylinositol 3-kinase (PI3K) have been shown to be implicated in the expression of several inflammatory target proteins. Here, we reported that LPS-induced up-regulation of VCAM-1 enhanced the adhesion of neutrophils onto HTSMC monolayer, which was inhibited by LY294002 and wortmannin. LPS stimulated phosphorylation of protein tyrosine kinases including Src, PYK2, and EGFR, which were further confirmed using specific anti-phospho-Src, PYK2, or EGFR Ab, respectively, revealed by Western blotting. LPS-stimulated Src, PYK2, EGFR, and Akt phosphorylation and VCAM-1 expression were attenuated by the inhibitors of Src (PP1), EGFR (AG1478), PI3-K (LY294002 and wortmannin), and Akt (SH-5), respectively, or transfection with siRNAs of Src or Akt and shRNA of p110. LPS-induced VCAM-1 expression was also blocked by pretreatment with curcumin (a p300 inhibitor) or transfection with p300 siRNA. LPS-stimulated Akt activation translocated into nucleus and associated with p300 and VCAM-1 promoter region was further confirmed by immunofluorescence, immunoprecipitation, and chromatin immunoprecipitation assays. This association of Akt and p300 to VCAM-1 promoter was inhibited by pretreatment with PP1, AG1478, wortmannin, and SH-5. LPS-induced p300 activation enhanced VCAM-1 promoter activity and VCAM-1 mRNA expression. These results suggested that in HTSMCs, Akt phosphorylation mediated through transactivation of Src/PYK2/EGFR promoted the transcriptional p300 activity and eventually led to VCAM-1 expression induced by LPS.</description><identifier>ISSN: 0041-008X</identifier><identifier>EISSN: 1096-0333</identifier><identifier>DOI: 10.1016/j.taap.2007.11.026</identifier><identifier>PMID: 18182168</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>60 APPLIED LIFE SCIENCES ; Akt ; Androstadienes - pharmacology ; Blotting, Western ; Cell Adhesion - drug effects ; Cell Line ; CHROMATIN ; Chromones - pharmacology ; CURCUMIN ; Dose-Response Relationship, Drug ; E1A-Associated p300 Protein - genetics ; E1A-Associated p300 Protein - metabolism ; EGFR ; HTSMCs ; Humans ; INFLAMMATION ; Lipopolysaccharides - pharmacology ; LPS ; MOLECULES ; Morpholines - pharmacology ; MUSCLES ; Myocytes, Smooth Muscle - cytology ; Myocytes, Smooth Muscle - drug effects ; Myocytes, Smooth Muscle - metabolism ; NEUTROPHILS ; Neutrophils - cytology ; Neutrophils - drug effects ; Neutrophils - metabolism ; p300 ; Phosphatidylinositol 3-Kinases - metabolism ; PHOSPHORYLATION ; Phosphorylation - drug effects ; PHOSPHOTRANSFERASES ; PROMOTERS ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; Quinazolines ; Receptor, Epidermal Growth Factor - metabolism ; RECEPTORS ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; RNA, Small Interfering - genetics ; Signal Transduction - drug effects ; Src ; src-Family Kinases - metabolism ; Trachea - cytology ; Transfection ; TYROSINE ; Tyrphostins - pharmacology ; Vascular Cell Adhesion Molecule-1 - genetics ; Vascular Cell Adhesion Molecule-1 - metabolism ; VCAM-1</subject><ispartof>Toxicology and applied pharmacology, 2008-04, Vol.228 (2), p.256-268</ispartof><rights>2007 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c328t-d31c02d9eb688e473bbb2590084360b54ede2c8841e8146c51b786e006c137103</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.taap.2007.11.026$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,777,781,882,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18182168$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://www.osti.gov/biblio/21140820$$D View this record in Osti.gov$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, Wei-Ning</creatorcontrib><creatorcontrib>Luo, Shue-Fen</creatorcontrib><creatorcontrib>Wu, Chou-Bing</creatorcontrib><creatorcontrib>Lin, Chih-Chung</creatorcontrib><creatorcontrib>Yang, Chuen-Mao</creatorcontrib><title>Lipopolysaccharide induces VCAM-1 expression and neutrophil adhesion to human tracheal smooth muscle cells: Involvement of Src/EGFR/PI3-K/Akt pathway</title><title>Toxicology and applied pharmacology</title><addtitle>Toxicol Appl Pharmacol</addtitle><description>In our previous study, LPS has been shown to induce vascular cell adhesion molecule-1(VCAM-1) expression through MAPKs and NF-κB in human tracheal smooth muscle cells (HTSMCs). In addition to these pathways, the non-receptor tyrosine kinases (Src), EGF receptor (EGFR), and phosphatidylinositol 3-kinase (PI3K) have been shown to be implicated in the expression of several inflammatory target proteins. Here, we reported that LPS-induced up-regulation of VCAM-1 enhanced the adhesion of neutrophils onto HTSMC monolayer, which was inhibited by LY294002 and wortmannin. LPS stimulated phosphorylation of protein tyrosine kinases including Src, PYK2, and EGFR, which were further confirmed using specific anti-phospho-Src, PYK2, or EGFR Ab, respectively, revealed by Western blotting. LPS-stimulated Src, PYK2, EGFR, and Akt phosphorylation and VCAM-1 expression were attenuated by the inhibitors of Src (PP1), EGFR (AG1478), PI3-K (LY294002 and wortmannin), and Akt (SH-5), respectively, or transfection with siRNAs of Src or Akt and shRNA of p110. LPS-induced VCAM-1 expression was also blocked by pretreatment with curcumin (a p300 inhibitor) or transfection with p300 siRNA. LPS-stimulated Akt activation translocated into nucleus and associated with p300 and VCAM-1 promoter region was further confirmed by immunofluorescence, immunoprecipitation, and chromatin immunoprecipitation assays. This association of Akt and p300 to VCAM-1 promoter was inhibited by pretreatment with PP1, AG1478, wortmannin, and SH-5. LPS-induced p300 activation enhanced VCAM-1 promoter activity and VCAM-1 mRNA expression. These results suggested that in HTSMCs, Akt phosphorylation mediated through transactivation of Src/PYK2/EGFR promoted the transcriptional p300 activity and eventually led to VCAM-1 expression induced by LPS.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>Akt</subject><subject>Androstadienes - pharmacology</subject><subject>Blotting, Western</subject><subject>Cell Adhesion - drug effects</subject><subject>Cell Line</subject><subject>CHROMATIN</subject><subject>Chromones - pharmacology</subject><subject>CURCUMIN</subject><subject>Dose-Response Relationship, Drug</subject><subject>E1A-Associated p300 Protein - genetics</subject><subject>E1A-Associated p300 Protein - metabolism</subject><subject>EGFR</subject><subject>HTSMCs</subject><subject>Humans</subject><subject>INFLAMMATION</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>LPS</subject><subject>MOLECULES</subject><subject>Morpholines - pharmacology</subject><subject>MUSCLES</subject><subject>Myocytes, Smooth Muscle - cytology</subject><subject>Myocytes, Smooth Muscle - drug effects</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>NEUTROPHILS</subject><subject>Neutrophils - cytology</subject><subject>Neutrophils - drug effects</subject><subject>Neutrophils - metabolism</subject><subject>p300</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>PHOSPHORYLATION</subject><subject>Phosphorylation - drug effects</subject><subject>PHOSPHOTRANSFERASES</subject><subject>PROMOTERS</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Quinazolines</subject><subject>Receptor, Epidermal Growth Factor - metabolism</subject><subject>RECEPTORS</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA, Small Interfering - genetics</subject><subject>Signal Transduction - drug effects</subject><subject>Src</subject><subject>src-Family Kinases - metabolism</subject><subject>Trachea - cytology</subject><subject>Transfection</subject><subject>TYROSINE</subject><subject>Tyrphostins - pharmacology</subject><subject>Vascular Cell Adhesion Molecule-1 - genetics</subject><subject>Vascular Cell Adhesion Molecule-1 - metabolism</subject><subject>VCAM-1</subject><issn>0041-008X</issn><issn>1096-0333</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2u0zAQRiME4pYLL8ACWUJil3YmdlMHsamqey8VRSD-xM5ynKniksTBdgp9EN6XhFZiB6uxRmc-6fNJkqcIcwTMF4d51LqfZwCrOeIcsvxeMkMo8hQ45_eTGYDAFEB-vUoehXAAgEIIfJhcoUSZYS5nya-d7V3vmlPQxtTa24qY7arBUGBfNuu3KTL62XsKwbqO6a5iHQ3Ru762DdNVTX_20bF6aPX48NrUpBsWWudizdohmIaYoaYJL9m2O7rmSC11kbk9--jN4ubu9sPi_Zanbxbrb5H1OtY_9Olx8mCvm0BPLvM6-Xx782nzOt29u9tu1rvU8EzGtOJoIKsKKnMpSax4WZbZshgbC55DuRRUUWakFEgSRW6WWK5kTgC5Qb5C4NfJ83OuC9GqYGwkUxvXdWSiyhAFyGyiXpyp3rvvA4WoWhumSrojNwS1AlFgkfP_giMkR3NiBLMzaLwLwdNe9d622p8UgprcqoOa3KrJrUJUo9vx6NklfShbqv6eXGSOwKszQOOXHS35qRF1hirrp0KVs__K_w3gubT8</recordid><startdate>20080415</startdate><enddate>20080415</enddate><creator>Lin, Wei-Ning</creator><creator>Luo, Shue-Fen</creator><creator>Wu, Chou-Bing</creator><creator>Lin, Chih-Chung</creator><creator>Yang, Chuen-Mao</creator><general>Elsevier Inc</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>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope><scope>OTOTI</scope></search><sort><creationdate>20080415</creationdate><title>Lipopolysaccharide induces VCAM-1 expression and neutrophil adhesion to human tracheal smooth muscle cells: Involvement of Src/EGFR/PI3-K/Akt pathway</title><author>Lin, Wei-Ning ; Luo, Shue-Fen ; Wu, Chou-Bing ; Lin, Chih-Chung ; Yang, Chuen-Mao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c328t-d31c02d9eb688e473bbb2590084360b54ede2c8841e8146c51b786e006c137103</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>60 APPLIED LIFE SCIENCES</topic><topic>Akt</topic><topic>Androstadienes - pharmacology</topic><topic>Blotting, Western</topic><topic>Cell Adhesion - drug effects</topic><topic>Cell Line</topic><topic>CHROMATIN</topic><topic>Chromones - pharmacology</topic><topic>CURCUMIN</topic><topic>Dose-Response Relationship, Drug</topic><topic>E1A-Associated p300 Protein - genetics</topic><topic>E1A-Associated p300 Protein - metabolism</topic><topic>EGFR</topic><topic>HTSMCs</topic><topic>Humans</topic><topic>INFLAMMATION</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>LPS</topic><topic>MOLECULES</topic><topic>Morpholines - pharmacology</topic><topic>MUSCLES</topic><topic>Myocytes, Smooth Muscle - cytology</topic><topic>Myocytes, Smooth Muscle - drug effects</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>NEUTROPHILS</topic><topic>Neutrophils - cytology</topic><topic>Neutrophils - drug effects</topic><topic>Neutrophils - metabolism</topic><topic>p300</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>PHOSPHORYLATION</topic><topic>Phosphorylation - drug effects</topic><topic>PHOSPHOTRANSFERASES</topic><topic>PROMOTERS</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Quinazolines</topic><topic>Receptor, Epidermal Growth Factor - metabolism</topic><topic>RECEPTORS</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA, Small Interfering - genetics</topic><topic>Signal Transduction - drug effects</topic><topic>Src</topic><topic>src-Family Kinases - metabolism</topic><topic>Trachea - cytology</topic><topic>Transfection</topic><topic>TYROSINE</topic><topic>Tyrphostins - pharmacology</topic><topic>Vascular Cell Adhesion Molecule-1 - genetics</topic><topic>Vascular Cell Adhesion Molecule-1 - metabolism</topic><topic>VCAM-1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, Wei-Ning</creatorcontrib><creatorcontrib>Luo, Shue-Fen</creatorcontrib><creatorcontrib>Wu, Chou-Bing</creatorcontrib><creatorcontrib>Lin, Chih-Chung</creatorcontrib><creatorcontrib>Yang, Chuen-Mao</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>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><collection>OSTI.GOV</collection><jtitle>Toxicology and applied pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Wei-Ning</au><au>Luo, Shue-Fen</au><au>Wu, Chou-Bing</au><au>Lin, Chih-Chung</au><au>Yang, Chuen-Mao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lipopolysaccharide induces VCAM-1 expression and neutrophil adhesion to human tracheal smooth muscle cells: Involvement of Src/EGFR/PI3-K/Akt pathway</atitle><jtitle>Toxicology and applied pharmacology</jtitle><addtitle>Toxicol Appl Pharmacol</addtitle><date>2008-04-15</date><risdate>2008</risdate><volume>228</volume><issue>2</issue><spage>256</spage><epage>268</epage><pages>256-268</pages><issn>0041-008X</issn><eissn>1096-0333</eissn><abstract>In our previous study, LPS has been shown to induce vascular cell adhesion molecule-1(VCAM-1) expression through MAPKs and NF-κB in human tracheal smooth muscle cells (HTSMCs). In addition to these pathways, the non-receptor tyrosine kinases (Src), EGF receptor (EGFR), and phosphatidylinositol 3-kinase (PI3K) have been shown to be implicated in the expression of several inflammatory target proteins. Here, we reported that LPS-induced up-regulation of VCAM-1 enhanced the adhesion of neutrophils onto HTSMC monolayer, which was inhibited by LY294002 and wortmannin. LPS stimulated phosphorylation of protein tyrosine kinases including Src, PYK2, and EGFR, which were further confirmed using specific anti-phospho-Src, PYK2, or EGFR Ab, respectively, revealed by Western blotting. LPS-stimulated Src, PYK2, EGFR, and Akt phosphorylation and VCAM-1 expression were attenuated by the inhibitors of Src (PP1), EGFR (AG1478), PI3-K (LY294002 and wortmannin), and Akt (SH-5), respectively, or transfection with siRNAs of Src or Akt and shRNA of p110. LPS-induced VCAM-1 expression was also blocked by pretreatment with curcumin (a p300 inhibitor) or transfection with p300 siRNA. LPS-stimulated Akt activation translocated into nucleus and associated with p300 and VCAM-1 promoter region was further confirmed by immunofluorescence, immunoprecipitation, and chromatin immunoprecipitation assays. This association of Akt and p300 to VCAM-1 promoter was inhibited by pretreatment with PP1, AG1478, wortmannin, and SH-5. LPS-induced p300 activation enhanced VCAM-1 promoter activity and VCAM-1 mRNA expression. These results suggested that in HTSMCs, Akt phosphorylation mediated through transactivation of Src/PYK2/EGFR promoted the transcriptional p300 activity and eventually led to VCAM-1 expression induced by LPS.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>18182168</pmid><doi>10.1016/j.taap.2007.11.026</doi><tpages>13</tpages></addata></record> |
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subjects | 60 APPLIED LIFE SCIENCES Akt Androstadienes - pharmacology Blotting, Western Cell Adhesion - drug effects Cell Line CHROMATIN Chromones - pharmacology CURCUMIN Dose-Response Relationship, Drug E1A-Associated p300 Protein - genetics E1A-Associated p300 Protein - metabolism EGFR HTSMCs Humans INFLAMMATION Lipopolysaccharides - pharmacology LPS MOLECULES Morpholines - pharmacology MUSCLES Myocytes, Smooth Muscle - cytology Myocytes, Smooth Muscle - drug effects Myocytes, Smooth Muscle - metabolism NEUTROPHILS Neutrophils - cytology Neutrophils - drug effects Neutrophils - metabolism p300 Phosphatidylinositol 3-Kinases - metabolism PHOSPHORYLATION Phosphorylation - drug effects PHOSPHOTRANSFERASES PROMOTERS Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Quinazolines Receptor, Epidermal Growth Factor - metabolism RECEPTORS Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics RNA, Messenger - metabolism RNA, Small Interfering - genetics Signal Transduction - drug effects Src src-Family Kinases - metabolism Trachea - cytology Transfection TYROSINE Tyrphostins - pharmacology Vascular Cell Adhesion Molecule-1 - genetics Vascular Cell Adhesion Molecule-1 - metabolism VCAM-1 |
title | Lipopolysaccharide induces VCAM-1 expression and neutrophil adhesion to human tracheal smooth muscle cells: Involvement of Src/EGFR/PI3-K/Akt pathway |
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