The Study of Cell Cycle Regulation and Epithelial-Mesenchymal Transition
The Study of Cell Cycle Regulation and Epithelial-Mesenchymal Transition
批准号:
18590844
负责人:
CHIDA Kingo
金额:
$2.17万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2006
资助国家:
日本
项目状态:
已结题
起止时间:
2006 至 2007
中文摘要
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英文摘要
Background: Epithelial mesenchymal transition (EMT) is known as the process by which differentiated epithelial cells undergo phenotypic transition to mesenchymal cells. Possibly, this process may occur in certain airway fibrotic diseases involving airway remodeling.Objectives: To clarify whether airway epithelial cells can differentiate mesenchymal cells through EMT.Methods: Mouse tracheal epithelial cells (mTEC) from BALB/c mouse were isolated, and cultured in an air-liquid interface (ALI) system in the presence or absence of TGF-p I. The expression of a-smooth muscle actin (a-SMA), vimentin, zonula occludens-I (Zo-I) and occludin was examined by immunofluorescence staining and westem blotting. Production of matrix metalloproteinase (MMP)-9 in culture medium was measured by enzyme linked immunosorbent assay.Results: Immunofluorescent staining revealed that TOF-p I treatment for 14 days induced the expression of mesenchymal markers, a-SMA and vimentin, and decreased the expression.of epithelial markers, Zo-1 and occluding in mTEC. Additionally, a-SMA and Zo-1 were colocalized within the single cells treated with TGF-(1l. In western blotting analysis, TGF-p1 treatment significantly enhanced the expression of a-SMA and vimentin, while it significantly reduced the expression of Zo-1 and occluding over time. Concentrations of MMP-9 in the culture medium were significantly higher in mTEC treated with TOF-β1 than those non-treated.Conclusions: These data suggest that EMT was induced by TGF-βl in the primary culture of mTEC with the ALI system, leading to the possibility that airway epithelial cells participates in airway remodeling through EMT.
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Correlation between peripheral blood T-cell profiles and airway inflammation in atopic asthma
特应性哮喘患者外周血 T 细胞谱与气道炎症的相关性
DOI:
--
发表时间:
2006
期刊:
J AIIergy Clin Immunol 118
影响因子:
--
作者:
[shirai, T., Suda, T., et. al.]
通讯作者:
et. al.
Japan idiopathic pulmonary fibrosis study group : Dietary fat and meat intake and idiopathic pulmonary fibrosis : a case-control study in Japan
日本特发性肺纤维化研究组:膳食脂肪和肉类摄入与特发性肺纤维化:日本的病例对照研究
DOI:
--
发表时间:
2006
期刊:
Int J tuber-lung dis 10(3)
影响因子:
--
作者:
[Sasaki, S., Yokoyama, T., Chida, K., Azuma, A., Suda, T., Kudoh, S., Sakamoto, N., Okamoto, K., Kobashi, G., Washfo, M., Inaba, Y., Tanaka, H]
通讯作者:
H
DOI:
10.1165/rcmb.2007-0237oc
发表时间:
2008-02-01
期刊:
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
影响因子:
6.4
作者:
[Naito, Tateaki, Suda, Takafumi, Nakamura, Hirotoshi]
通讯作者:
Nakamura, Hirotoshi
Immunization with dendritic cells retrovirally transduced with mycobacterial antigen 85A gene elicits the specific cellular immunity including cytotoxic T-lymphocyte activity specific to an epitope on antigen 85A
用分枝杆菌抗原 85A 基因逆转录病毒转导的树突状细胞进行免疫可引发特异性细胞免疫,包括对抗原 85A 上的表位具有特异性的细胞毒性 T 淋巴细胞活性
DOI:
--
发表时间:
期刊:
Vaccine 出版中
影响因子:
--
作者:
[Ansari AA, Mayne AE, Onlamoon N, Pattanapanyasat K, Mori K, Villinger F., 大友一雄, 大友一雄, 大友 一雄, 五島 敏芳, 神立 孝一, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司, 岡田全司]
通讯作者:
岡田全司
DOI:
10.1111/j.1532-5415.2006.00825.x
发表时间:
2006-08-01
期刊:
JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
影响因子:
6.3
作者:
[Naito, Tateaki, Suda, Takafumi, Nakamura, Hirotoshi]
通讯作者:
Nakamura, Hirotoshi
共 20 条
The study on administration route of T-cell independent vaccinefrom the point view of bronchus-associated lymphoid tissue
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批准号:22590855
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.75万
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财政年份:2010
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负责人:CHIDA Kingo
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依托单位:
Immunohistochemical study of cell cycle regulators in idiopathic pulmonary fibrosis
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批准号:15590802
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$1.86万
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财政年份:2003
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负责人:CHIDA Kingo
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依托单位:
The significance of expression of CD1 family by dendritic cells in human sarcoid lesions
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批准号:13670594
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$1.41万
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财政年份:2001
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负责人:CHIDA Kingo
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依托单位:
A Monoclonal Antibody Directed Against Activation Antigen on Alveolar Macrophages.
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批准号:01570427
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项目类别:Grant-in-Aid for General Scientific Research (C)
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资助金额:$1.22万
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财政年份:1989
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负责人:CHIDA Kingo
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依托单位:
海外基金