کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5860579 | 1133201 | 2013 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Mechanism of E-cadherin redistribution in bronchial airway epithelial cells in a TDI-induced asthma model
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کلمات کلیدی
ERKTDIHBEHDMTSLPE-cadherin - E-CadherinTJs - TJSAsthma - آسمtight junctions - اتصالات محکمhuman bronchial epithelial - اپیتلیال برونشیت انسانtoluene diisocyanate - تولئین دی ایزوسیاناتzonula occludens - شل بستنThymic stromal lymphopoietin - لنفوپیتین استروما تیمیکextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیHouse dust mite - گرد و غبار خانه
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Mechanism of E-cadherin redistribution in bronchial airway epithelial cells in a TDI-induced asthma model Mechanism of E-cadherin redistribution in bronchial airway epithelial cells in a TDI-induced asthma model](/preview/png/5860579.png)
چکیده انگلیسی
E-cadherin (epithelial cadherin), a transmembrane protein, provides essential architecture and immunological function to the airway epithelium, a barrier structure that plays an essential role in asthma pathogenesis. Toluene diisocyanate (TDI) is currently one of the leading causes of occupational asthma. However, relatively few studies have been undertaken to determine the biological effects of TDI on the barrier properties of airway epithelium, but it is known that TDI can damage airway epithelial tight junctions in vitro. Here, we hypothesize that TDI can injure E-cadherin both in normal and allergic-induced airway epithelium. To test this, we developed a murine model of TDI-induced asthma characterized by neutrophil-dominated airway inflammation, epithelial shedding, and obvious aberrant distribution of E-cadherin. Pretreatment with dexamethasone (DEX) significantly rescued the immunoreactivity of E-cadherin, accompanied by increased neutrophils in bronchoalveolar lavage fluid (BALF). In vitro, TDI-human serum albumin (HSA)-induced redistribution of E-cadherin was associated with extracellular signal-regulated kinase (ERK)1/2 activation. The inhibition of phospho-ERK (p-ERK)1/2 by DEX can partly reverse this reaction. These results indicate that E-cadherin redistribution may be an important contributor in the generation of TDI-induced asthma.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology Letters - Volume 220, Issue 1, 20 June 2013, Pages 8-14
Journal: Toxicology Letters - Volume 220, Issue 1, 20 June 2013, Pages 8-14
نویسندگان
Jiafu Song, Haijin Zhao, Hangming Dong, Dandan Zhang, Mengchen Zou, Haixiong Tang, Laiyu Liu, Zhenyu Liang, Yanhua Lv, Fei Zou, Shaoxi Cai,