Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 오재원 | - |
dc.date.accessioned | 2018-03-15T05:38:04Z | - |
dc.date.available | 2018-03-15T05:38:04Z | - |
dc.date.issued | 2014-07 | - |
dc.identifier.citation | Plos One, Jul 21, 2014, 9(7), e102373 | en_US |
dc.identifier.issn | 1932-6203 | - |
dc.identifier.uri | http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0102373 | - |
dc.description.abstract | Epidemiological evidence suggests that obesity is associated with inflammation of the respiratory tract and the pathogenesis of asthma. The purpose of this study was to examine the role of phospholipase D1 (PLD1) in leptin-induced expression of the proinflammatory cytokine, tumor necrosis factor (TNF)-alpha, and to suggest a molecular link between obesity and respiratory tract inflammation. We investigated whether leptin, a typical adipocytokine, plays a role in the expression of TNF-alpha through increased PLD1 activity in Raw 264.7. Leptin enhanced the activity of PLD1 through activation of PLC gamma and Src, while PLD1 siRNA decreased the leptin-induced expression and production of TNF-alpha. Leptin-induced PLD activation was also inhibited by a PLCc inhibitor (PAO) and Src kinase inhibitor (PP2), indicating that PLCc and Src kinase are upstream activators of PLD1. Down-regulation of PLD1 also completely blocked activation of p70S6K, an activator of JNK. Leptin-induced expression of TNF-alpha was also prevented by inhibition of p70S6K and JNK. Taken together, these results indicate that PLD1 acts as an important regulator of leptin-induced expression of TNF-alpha by participating in the PLCc/Src/PLD1/PA/ p70S6K/JNK pathway. | en_US |
dc.description.sponsorship | This study was supported by the Korea Science and Engineering Foundation (NRF-2012R1A5A2A34671243) through the Medical Research Center at Hanyang University College of Medicine, Republic of Korea, and the National Research Foundation of Korea (NRF), funded by the Mid-career Researcher Program (NRF-2010-0026844). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. | en_US |
dc.language.iso | en | en_US |
dc.publisher | Public Library Science | en_US |
dc.subject | HUMAN ENDOTHELIAL-CELLS | en_US |
dc.subject | INDUCED NEURITE OUTGROWTH | en_US |
dc.subject | TUMOR-NECROSIS-FACTOR | en_US |
dc.subject | KAPPA-B ACTIVATION | en_US |
dc.subject | P70 S6 KINASE | en_US |
dc.subject | PROTEIN-KINASE | en_US |
dc.subject | MAMMALIAN TARGET | en_US |
dc.subject | DENDRITIC CELLS | en_US |
dc.subject | BODY-WEIGHT | en_US |
dc.subject | H19-7 CELLS | en_US |
dc.title | Leptin Increases TNF-alpha Expression and Production through Phospholipase D1 in Raw 264.7 Cells | en_US |
dc.type | Article | en_US |
dc.relation.no | 7 | - |
dc.relation.volume | 9 | - |
dc.identifier.doi | 10.1371/journal.pone.0102373 | - |
dc.relation.page | 0-0 | - |
dc.relation.journal | PLOS ONE | - |
dc.contributor.googleauthor | Choi, Hye-Jin | - |
dc.contributor.googleauthor | Oh, Cheong-Hae | - |
dc.contributor.googleauthor | Han, Joong-Soo | - |
dc.contributor.googleauthor | Lee, Se-Min | - |
dc.contributor.googleauthor | Oh, Jae-Won | - |
dc.relation.code | 2014037807 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | jaewonoh | - |
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