Apoptosis inhibitor of macrophage (AIM) expression in alveolar macrophages in COPD
| العنوان: | Apoptosis inhibitor of macrophage (AIM) expression in alveolar macrophages in COPD |
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| المؤلفون: | Makoto Odaka, Keisuke Saito, Jun Araya, Chikako Tsurushige, Naoki Takasaka, Satoko Arai, Hiromichi Hara, Satoko Fujii, Kenji Kobayashi, Makoto Kawaishi, Noriki Kamiya, Katsutoshi Nakayama, Yumi Kaneko, Jun-ichi Kojima, Jun Hirano, Takanori Numata, Takeo Ishikawa, Hiroshi Hano, Toru Miyazaki, Toshiaki Morikawa, Saburo Ito, Kazuyoshi Kuwano, Kenichiro Shimizu |
| المصدر: | Respiratory Research |
| بيانات النشر: | BioMed Central, 2013. |
| سنة النشر: | 2013 |
| مصطلحات موضوعية: | Pulmonary and Respiratory Medicine, Antigens, Differentiation, T-Lymphocyte, Male, Apoptosis Inhibitor, Apoptosis, Biology, Alveolar macrophage, Pulmonary Disease, Chronic Obstructive, Antigens, CD, Macrophages, Alveolar, medicine, Macrophage, AIM, COPD, Humans, Lectins, C-Type, Cells, Cultured, Aged, medicine.diagnostic_test, U937 cell, Research, U937 Cells, Middle Aged, medicine.disease, Bronchoalveolar lavage, HEK293 Cells, Gene Expression Regulation, Immunology, Female, Apoptosis Regulatory Proteins, Bronchoalveolar Lavage Fluid, Immunostaining |
| الوصف: | Background 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. Methods 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. Results 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. Conclusions These results suggest that AIM expression in association with cigarette smoking may be involved in accumulation of AM in COPD. |
| اللغة: | English |
| تدمد: | 1465-993X 1465-9921 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::eaf24e24767eaf7b656214768de77281Test http://europepmc.org/articles/PMC3599155Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....eaf24e24767eaf7b656214768de77281 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 1465993X 14659921 |
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