کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10904018 | 1086551 | 2014 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Induction of galectin-1 by TGF-β1 accelerates fibrosis through enhancing nuclear retention of Smad2
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کلمات کلیدی
ERKTGF-βp-Smad2TDGCol1a2TGFECLBLMPI3KHRPFBSSDSPBSDMEMBSA - BSADulbecco׳s modified Eagle׳s medium - Dilbecco's modified Eagle's mediumH&E - H & EMAPK - MAPKbovine serum albumin - آلبومین سرم گاوstandard deviations - انحراف معیارBleomycin - بلئومایسینenhanced chemiluminescence - بهبود شیمیایی لومنtransforming growth factor - تبدیل فاکتور رشدfetal bovine serum - سرم جنین گاوPhosphate buffered saline - فسفات بافر شورPhosphatidyl Inositol 3-kinase - فسفاتیدیل آنزیم 3-کینازFibrosis - فیبروز یا فساد الیافwild-type - نوع وحشیHematoxylin and Eosin - هماتوکسیلین و ائوزینHorseradish peroxidase - پراکسیداز هوررادیشmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenCollagen - کلاژنcol - کولextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیGal-3 - گال سومGal-1 - گال-1Galectin-1 - گالکتین-1Galectin-3 - گالکتین-3
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Fibrosis is one of the most serious side effects in cancer patients undergoing radio-/ chemo-therapy, especially of the lung, pancreas or kidney. Based on our previous finding that galectin-1 (Gal-1) was significantly increased during radiation-induced lung fibrosis in areas of pulmonary fibrosis, we herein clarified the roles and action mechanisms of Gal-1 during fibrosis. Our results revealed that treatment with TGF-β1 induced the differentiation of fibroblast cell lines (NIH3T3 and IMR-90) to myofibroblasts, as evidenced by increased expression of the fibrotic markers smooth muscle actin-alpha (α-SMA), fibronectin, and collagen (Col-1). We also observed marked and time-dependent increases in the expression level and nuclear accumulation of Gal-1. The TGF-β1-induced increases in Gal-1, α-SMA and Col-1 were decreased by inhibitors of PI3-kinase and p38 MAPK, but not ERK. Gal-1 knockdown using shRNA decreased the phosphorylation and nuclear retention of Smad2, preventing the differentiation of fibroblasts. Gal-1 interacted with Smad2 and phosphorylated Smad2, which may accelerate fibrotic processes. In addition, up-regulation of Gal-1 expression was demonstrated in a bleomycin (BLM)-induced mouse model of lung fibrosis in vivo. Together, our results indicate that Gal-1 may promote the TGF-β1-induced differentiation of fibroblasts by sustaining nuclear localization of Smad2, and could be a potential target for the treatment of pulmonary fibrotic diseases.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Cell Research - Volume 326, Issue 1, 1 August 2014, Pages 125-135
Journal: Experimental Cell Research - Volume 326, Issue 1, 1 August 2014, Pages 125-135
نویسندگان
Min Jin Lim, Jiyeon Ahn, Jae Youn Yi, Mi-Hyoung Kim, A-Rang Son, Sae-lo-oom Lee, Dae-Seog Lim, Sung Soo Kim, Mi Ae Kang, Youngsoo Han, Jie-Young Song,