Source:http://linkedlifedata.com/resource/pubmed/id/21268080
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rdf:type | |
lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0040578,
umls-concept:C0068355,
umls-concept:C0085828,
umls-concept:C0086418,
umls-concept:C0185117,
umls-concept:C0239059,
umls-concept:C0752312,
umls-concept:C0851285,
umls-concept:C1135918,
umls-concept:C1333201,
umls-concept:C1333336,
umls-concept:C1370600,
umls-concept:C1555707,
umls-concept:C1705851,
umls-concept:C2752151,
umls-concept:C2828366,
umls-concept:C2911684
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pubmed:issue |
2
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pubmed:dateCreated |
2011-1-26
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pubmed:abstractText |
Up-regulation of cytosolic phospholipase A(2) (cPLA(2)) by cigarette smoke extract (CSE) may play a critical role in airway inflammatory diseases. However, the mechanisms underlying CSE-induced cPLA(2) expression in human tracheal smooth muscle cells (HTSMCs) were not completely understood. Here, we demonstrated that CSE-induced cPLA(2) protein and mRNA expression was inhibited by pretreatment with the inhibitors of AP-1 (tanshinone IIA) and p300 (garcinol) or transfection with siRNAs of c-Jun, c-Fos, and p300. Moreover, CSE also induced c-Jun and c-Fos expression, which were inhibited by pretreatment with the inhibitors of NADPH oxidase (diphenyleneiodonium chloride and apocynin) and the ROS scavenger (N-acetyl-L-cysteine) or transfection with siRNAs of p47(phox) and NADPH oxidase (NOX)2. CSE-induced c-Fos expression was inhibited by pretreatment with the inhibitors of MEK1 (U0126) and p38 MAPK (SB202190) or transfection with siRNAs of p42 and p38. CSE-induced c-Jun expression and phosphorylation were inhibited by pretreatment with the inhibitor of JNK1/2 (SP600125) or transfection with JNK2 siRNA. CSE-stimulated p300 phosphorylation was inhibited by pretreatment with the inhibitors of NADPH oxidase and JNK1/2. Furthermore, CSE-induced p300 and c-Jun complex formation was inhibited by pretreatment with diphenyleneiodonium chloride, apocynin, N-acetyl-L-cysteine or SP600125. These results demonstrated that CSE-induced cPLA(2) expression was mediated through NOX2-dependent p42/p44 MAPK and p38 MAPK/c-Fos and JNK1/2/c-Jun/p300 pathways in HTSMCs.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/E1A-Associated p300 Protein,
http://linkedlifedata.com/resource/pubmed/chemical/EP300 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/NADPH Oxidase,
http://linkedlifedata.com/resource/pubmed/chemical/Phospholipases A2, Cytosolic,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor AP-1
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1097-4644
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pubmed:author | |
pubmed:copyrightInfo |
Copyright © 2010 Wiley-Liss, Inc.
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pubmed:issnType |
Electronic
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pubmed:volume |
112
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
589-99
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pubmed:meshHeading |
pubmed-meshheading:21268080-Blotting, Western,
pubmed-meshheading:21268080-Cell Line,
pubmed-meshheading:21268080-E1A-Associated p300 Protein,
pubmed-meshheading:21268080-Humans,
pubmed-meshheading:21268080-Immunoprecipitation,
pubmed-meshheading:21268080-Mitogen-Activated Protein Kinases,
pubmed-meshheading:21268080-Myocytes, Smooth Muscle,
pubmed-meshheading:21268080-NADPH Oxidase,
pubmed-meshheading:21268080-Phospholipases A2, Cytosolic,
pubmed-meshheading:21268080-RNA, Small Interfering,
pubmed-meshheading:21268080-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:21268080-Smoking,
pubmed-meshheading:21268080-Trachea,
pubmed-meshheading:21268080-Transcription Factor AP-1
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pubmed:year |
2011
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pubmed:articleTitle |
Cigarette smoke extract regulates cytosolic phospholipase A2 expression via NADPH oxidase/MAPKs/AP-1 and p300 in human tracheal smooth muscle cells.
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pubmed:affiliation |
Department of Physiology and Pharmacology, Chang Gung University, Kwei-San, Tao-Yuan, Taiwan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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