کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8259686 | 1534643 | 2015 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Crosstalk between calpain activation and TGF-β1 augments collagen-I synthesis in pulmonary fibrosis
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کلمات کلیدی
ECMTGF-β1IPFp-Smad2/3SMADphosphorylated-AKTp-Akt - P-AKTELISA - تست الیزاEnzyme-linked immunosorbent assay - تست الیزاFibroblasts - فیبروبلاست هاHuman lung fibroblasts - فیبروبلاست های انسانی ریهPulmonary fibrosis - فیبروز ریهidiopathic pulmonary fibrosis - فیبروز ریوی ایدیوپاتیکExtracellular matrix - ماتریکس خارج سلولیCalpain - کالپینCollagen - کلاژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Crosstalk between calpain activation and TGF-β1 augments collagen-I synthesis in pulmonary fibrosis Crosstalk between calpain activation and TGF-β1 augments collagen-I synthesis in pulmonary fibrosis](/preview/png/8259686.png)
چکیده انگلیسی
Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease of unknown cause that typically leads to respiratory failure and death within 3-5 years of diagnosis. TGF-β1 is considered a major profibrotic factor. However, TGF-β1 is necessary but not sufficient to the pathogenesis of fibrotic lesion of the lungs. Recent observations have revealed that calpain, a calcium dependent protease, plays a pivotal role in tissue remodeling and fibrosis. However, the mechanism of calpain mediating pulmonary fibrosis is not understood. Calpain conditional knockout (ER-Cre+/âcapns1flox/flox) mice and primary human lung fibroblasts (HLFs) were used here to investigate the relationship between calpain and TGF-β1. Calpain knockout mice were protected from fibrotic effects of bleomycin. Bleomycin induced increases in TGF-β1 via calpain activation in HLFs. Moreover, TGF-β1 also activated calpain. This crosstalk between calpain activation and TGF-β1 triggered the downstream signaling pathway including TGF-β1 Smad2/3 and non-Smad (Akt) pathways, as well as collagen-I synthesis. Taken together, our data indicate that the crosstalk between calpain activation and TGF-β1 augments collagen-I synthesis in HLFs and in pulmonary fibrosis. Intervention in the crosstalk between calpain activation and TGF-β1 is a novel potential strategy to prevent pulmonary fibrosis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1852, Issue 9, September 2015, Pages 1796-1804
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1852, Issue 9, September 2015, Pages 1796-1804
نویسندگان
Feng-Zhi Li, Peng-Cheng Cai, Lin-Jie Song, Li-Ling Zhou, Qian Zhang, Shan-Shan Rao, Yu Xia, Fei Xiang, Jian-Bao Xin, Peter A. Greer, Huan-Zhong Shi, Yunchao Su, Wan-Li Ma, Hong Ye,