کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2131706 1086655 2008 12 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
TGFβ stimulated re-epithelialisation is regulated by CTGF and Ras/MEK/ERK signalling
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی تحقیقات سرطان
پیش نمایش صفحه اول مقاله
TGFβ stimulated re-epithelialisation is regulated by CTGF and Ras/MEK/ERK signalling
چکیده انگلیسی

The complex mechanisms by which transforming growth factor β (TGFβ) regulate re-epithelialisation following injury of stratified epithelia are not fully understood. TGFβ signals via binding to distinct receptors activating downstream effectors, including Smads which initiate transcription of target genes. However, studies have shown that TGFβ can also signal independently of Smads through MAPK pathways, demonstrating the diversity of TGFβ signalling. Connective tissue growth factor (CTGF) is strongly induced by and acts downstream of TGFβ causing pathophysiology in tissues by inducing matrix deposition, conversion of fibroblasts into contractile myofibroblasts (e.g. dermis and corneal stroma) and stimulation of epithelial-to-mesenchymal transition (e.g. kidney and lung) all of which are known to cause fibrosis. However, a role for CTGF in epithelial cell function which does not involve direct contribution to fibrosis has not been demonstrated. We show for the first time that synthesis of CTGF in cultures of human corneal epithelial cells is induced by TGFβ through the Ras/MEK/ERK MAPK signalling pathway and that this is required for re-epithelialisation to occur through cell migration. These data reveal a novel function for CTGF in the regulation of epithelial tissue repair beyond its established role in fibrosis, and further highlight the complexity of TGFβ regulation of epithelial cell function.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Cell Research - Volume 314, Issue 1, 1 January 2008, Pages 131–142
نویسندگان
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