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2017 Fiscal Year Final Research Report

Regulation of mucus secretion in ACO

Research Project

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Project/Area Number 15K09183
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Respiratory organ internal medicine
Research InstitutionYokohama City University

Principal Investigator

SHINKAI Masaharu  横浜市立大学, 医学部, 准教授 (10535214)

Co-Investigator(Kenkyū-buntansha) 金子 猛  横浜市立大学, 医学研究科, 教授 (90275066)
下川路 伊亮  横浜市立大学, 附属市民総合医療センター, 助教 (70751634)
Project Period (FY) 2015-04-01 – 2018-03-31
Keywords気管支喘息 / 慢性閉塞性肺疾患 / IL-13 / TGFα / anoctamin-1 / CLCA-1
Outline of Final Research Achievements

Compared with their counterparts with asthma or COPD alone, patients with ACO have significantly increased risk of exacerbations and worse respiratory symptoms. Activation of the interleukin-13 (IL-13) receptor leads to signal transducer and induction of chloride channel accessory 1 (CLCA1) and anoctamin-1(ANO1), increasing secretion of the gel-forming mucin MUC5AC. Activation of TGFα also leads to MUC5AC production via extracellular signal-regulated kinase (ERK1/2). We examined the effect of both IL-13 and TGFα signaling leading to mucin production. Histochemical analysis was performed using hematoxylin and eosin (HE) staining and MUC5AC immunostaining. MUC5AC, ANO1 and CLCA1 mRNA expression were evaluated by real-time PCR. Western analysis was used to assess phosphorylation. Our data suggest that the effect of both IL-13 and TGFα signaling increased mucus secretion perhaps via cross talk among cell-signaling transduction pathways.

Free Research Field

呼吸器内科学

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Published: 2019-03-29  

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