Apoptosis inhibitor of macrophage (AIM) expression in alveolar macrophages in COPD.
Apoptosis inhibitor of macrophage (AIM) expression in alveolar macrophages in COPD.
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DOI：
10.1186/1465-9921-14-30
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发表时间：
2013-03-05
影响因子：
5.8
通讯作者：
Kuwano K
中科院分区：
文献类型：
--
作者：
Kojima J;Araya J;Hara H;Ito S;Takasaka N;Kobayashi K;Fujii S;Tsurushige C;Numata T;Ishikawa T;Shimizu K;Kawaishi M;Saito K;Kamiya N;Hirano J;Odaka M;Morikawa T;Hano H;Arai S;Miyazaki T;Kaneko Y;Nakayama K;Kuwano K
肺泡巨噬细胞（AM）凋亡抵抗导致的AM大量聚集参与了慢性阻塞性肺疾病（COPD）的发病机制。巨噬细胞凋亡抑制剂（AIM），已被证明是由成熟的组织巨噬细胞产生的，AIM对多种诱导凋亡的刺激表现出抗凋亡特性。因此，我们试图确定AIM是否在AM中表达，以及AIM是否参与香烟烟雾提取物（CSE）暴露背景下细胞凋亡的调节。进行AIM的免疫组织化学评价。通过计数每个病例中的总AM数和阳性染色AM数来评估免疫染色（对照组中n = 5，非COPD吸烟者中n = 5，COPD中n = 5）。从支气管肺泡灌洗液（BALF）中分离AM。评价AM中AIM表达水平响应于CSE暴露的变化。通过siRNA转染介导抗凋亡Bcl-xL的敲低。采用U937单核巨噬细胞系研究AIM的抗凋亡作用。COPD肺AM及AM阳性细胞数明显增多。AIM表达在mRNA和蛋白质水平在孤立的AM，这是增强响应CSE暴露。AIM可显著增加AM中Bcl-xL的表达，Bcl-xL参与了AIM在CSE作用下抗U937细胞凋亡的部分机制。这些结果表明，AIM表达与吸烟可能参与了AM在COPD中的积累。
Marked accumulation of alveolar macrophages (AM) conferred by apoptosis resistance has been implicated in pathogenesis of chronic obstructive pulmonary disease (COPD). Apoptosis inhibitor of macrophage (AIM), has been shown to be produced by mature tissue macrophages and AIM demonstrates anti-apoptotic property against multiple apoptosis-inducing stimuli. Accordingly, we attempt to determine if AIM is expressed in AM and whether AIM is involved in the regulation of apoptosis in the setting of cigarette smoke extract (CSE) exposure. Immunohistochemical evaluations of AIM were performed. Immunostaining was assessed by counting total and positively staining AM numbers in each case (n = 5 in control, n = 5 in non-COPD smoker, n = 5 in COPD). AM were isolated from bronchoalveolar lavage fluid (BALF). The changes of AIM expression levels in response to CSE exposure in AM were evaluated. Knock-down of anti-apoptotic Bcl-xL was mediated by siRNA transfection. U937 monocyte-macrophage cell line was used to explore the anti-apoptotic properties of AIM. The numbers of AM and AIM-positive AM were significantly increased in COPD lungs. AIM expression was demonstrated at both mRNA and protein levels in isolated AM, which was enhanced in response to CSE exposure. AIM significantly increased Bcl-xL expression levels in AM and Bcl-xL was involved in a part of anti-apoptotic mechanisms of AIM in U937 cells in the setting of CSE exposure. These results suggest that AIM expression in association with cigarette smoking may be involved in accumulation of AM in COPD.
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DOI：
10.4049/jimmunol.0900473
发表时间：
2009-08-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Shaykhiev R;Krause A;Salit J;Strulovici-Barel Y;Harvey BG;O'Connor TP;Crystal RG
通讯作者：
Crystal RG
DOI：
10.1164/rccm.200811-1757st
发表时间：
2010-09-01
影响因子：
24.7
作者：
Eisner, Mark D.;Anthonisen, Nicholas;Balmes, John R.
通讯作者：
Balmes, John R.
DOI：
10.1152/ajplung.00422.2001
发表时间：
2002-10-01
影响因子：
4.9
作者：
Araya, J;Maruyama, M;Kobayashi, M
通讯作者：
Kobayashi, M
影响因子：
9.6
作者：
Ohar, Jill A.;Hamilton, Raymond E., Jr.;Holian, Andrij
通讯作者：
Holian, Andrij
影响因子：
7.1
作者：
van den Borst, Bram;Gosker, Harry R.;Schols, Annemie M. W. J.
通讯作者：
Schols, Annemie M. W. J.