کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10770861 | 1050836 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cigarette smoke condensate induces MMP-12 gene expression in airway-like epithelia
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کلمات کلیدی
AP-1Epithelial - اپیتلیالNADPH oxidase - اکسیداز NADPH Oxidants - اکسیدان هاBronchial - برونشChronic obstructive pulmonary disease - بیماری مزمن انسدادی ریهCigarette smoke - دود سیگارTNF-α - فاکتور نکروز توموری آلفاMatrix metalloproteinase-12 - ماتریکس متالوپروتئیناز-12air-liquid Interface - هوا مایع رابط
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Cigarette smoke (CS)-induced emphysema is attributable to matrix metalloproteinase-12 (MMP-12) in mice, however, a relationship between CS and MMP-12 is absent in human emphysema. Here, we show that cigarette smoke condensate (CSC) induces MMP-12 gene expression in airway-like epithelia through a hydrogen peroxide (H2O2)-dependent pathway involving NADPH oxidase, AP-1, and TNF-α. Cigarette smoke condensate-induced H2O2 production and MMP-12 gene expression were inhibited by apocynin, a specific inhibitor of NADPH oxidases, while 3-aminobenzamide, an inhibitor of AP-1, attenuated CSC-induced MMP-12 gene expression. Messenger RNAs encoding phagocytic NADPH oxidase components and a homologue of p67phox, p51 (NOXA1), were detected, while mRNA of dual oxidase (Duox)1 was unchanged by CSC. Enbrel, an inhibitor of TNF-α function, reduced CSC-induced H2O2 production and MMP-12 expression. These findings provide novel evidence of a direct relationship between CS exposure and MMP-12 in human airway epithelia and suggest several targets for modulation of this potentially pathogenic pathway.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 330, Issue 1, 29 April 2005, Pages 194-203
Journal: Biochemical and Biophysical Research Communications - Volume 330, Issue 1, 29 April 2005, Pages 194-203
نویسندگان
Mark C. Lavigne, Michael J. Eppihimer,