2016 Fiscal Year Final Research Report
The crucial role of PLCepsilon in a mouse model of acute lung injury
| Project/Area Number |
26461188
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Kobe University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | PLCε / ALI |
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| Outline of Final Research Achievements |
Phospholipase Cε (PLCε) is an effector of Ras and Rap small GTPases. The aim of this study is to examine whether PLCε is involved also in the pathogenesis of neutrophil-mediated airway inflammation. Acute lung injury (ALI) was experimentally induced by intratracheal administration of LPS in PLCε knock out (KO) mice. In contrast with PLCε wild type (WT) mice, the accumulation of inflammatory cells in the alveolar space were substantially reduced in PLC KO mice. Comparison of the cytokine mRNA levels of the total lungs by qRT-PCR of LPS-stimulated mice indicated that PLCε deficiency attenuated the LPS-induced expression of the CXC family chemokines. These results suggest that PLCε mediated induction of the CXC family chemokines by the structural cells plays an important role in neutrophil mediated airway inflammation and that PLCε could be a molecular target for the treatment of patients with ARDS.
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| Free Research Field |
呼吸器内科学
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