کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5500951 | 1534620 | 2017 | 42 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Rac1 signaling regulates cigarette smoke-induced inflammation in the lung via the Erk1/2 MAPK and STAT3 pathways
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
NF-κBIL-6STAT3JnkCSENSC16HBEIL-8Rac1c-Jun N-terminal kinases - C-Jun N-terminal kinasesERK1/2 - ERK1 / 2MAPK - MAPKSmall interfering RNA - RNA تداخل کوچکsiRNA - siRNAPulmonary inflammation - التهاب ریهInterleukin-8 - اینترلوکین -8interleukin-6 - اینترلوکین ۶COPD - بیماری مزمن انسدادی ریهChronic obstructive pulmonary disease - بیماری مزمن انسدادی ریهCigarette smoke - دود سیگارHuman bronchial epithelial cell - سلول اپیتلیال برونش انسانcigarette smoke extract - عصاره سیگار سیگارnuclear factor-κB - فاکتور هسته ای κBbronchoalveolar lavage fluids - مایعات لارو برونکلو فلزیSignal transducer and activator of transcription-3 - مبدل سیگنال و فعال کننده رونویسی 3extracellular regulated protein kinases - پروتئین کیناز تنظیم شده خارج سلولیmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenKeratinocyte-derived chemokine - کومکتین مشتق شده از کراتینوسیت
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Cigarette smoke (CS) is a major risk factor for the development of chronic obstructive pulmonary disease (COPD). Our previous studies have indicated that Rac1 is involved in lipopolysaccharide-induced pulmonary injury and CS-mediated epithelial-mesenchymal transition. However, the contribution of Rac1 activity to CS-induced lung inflammation remains not fully clear. In this study, we investigated the regulation of Rac1 in CS-induced pulmonary inflammation. Mice or 16HBE cells were exposed to CS or cigarette smoke extract (CSE) to induce acute inflammation. The lungs of mice exposed to CS showed an increase in the release of interleukin-6 (IL-6) and keratinocyte-derived chemokine (KC), as well as an accumulation of inflammatory cells, indicating high Rac1 activity. The exposure of 16HBE cells to CSE resulted in elevated Rac1 levels, as well as increased release of IL-6 and interleukin-8 (IL-8). Selective inhibition of Rac1 ameliorated the release of IL-6 and KC as well as inflammation in the lungs of CS-exposed mice. Histological assessment showed that treatment with a Rac1 inhibitor, NSC23766, led to a decrease in CD68 and CD11b positive cells and the infiltration of neutrophils and macrophages into the alveolar spaces. Selective inhibition or knockdown of Rac1 decreased IL-6 and IL-8 release in 16HBE cells induced by CSE, which correlated with CSE-induced Rac1-regulated Erk1/2 mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription-3 (STAT3) signaling. Our data suggest an important role for Rac1 in the pathological alterations associated with CS-mediated inflammation. Rac1 may be a promising therapeutic target for the treatment of CS-induced pulmonary inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1863, Issue 7, July 2017, Pages 1778-1788
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1863, Issue 7, July 2017, Pages 1778-1788
نویسندگان
Jun-xia Jiang, Shui-juan Zhang, Hui-juan Shen, Yan Guan, Qi Liu, Wei Zhao, Yong-liang Jia, Jian Shen, Xiao-feng Yan, Qiang-min Xie,