Transforming growth factor (TGF) family members play an important role in the regulation of the integrity of the cornea, and the pathogenesis of fibrosis cornea. Currently, there are no effective agents targeting TGF-β signaling to reduce corneal fibrosis. Glucosamine (GlcN), which are widely used in the treatment of osteoarthritis, cancel the morphological effects of TGF-β2 in the cells of the retinal pigmented epithelium in disease model mice. Here, we sought to determine whether GlcN will provide beneficial effects on TGF-β1-induced corneal fibrosis.
In human corneal fibroblasts (HCF) is treated with GlcN, expression Krüppel-like factor 4 (KLF4) and downstream signaling effects specified in presence and absence of TGF-β1 using immunoblot analysis. We further explored GlcN inhibition of fibroblast-to-myofibroblast differentiation through KLF4 siRNA. Effect of cycloheximide on protein levels of KLF4 with or without the administration of GlcN assessed to determine whether KLF4 protein.In GlcN affect the stability of health-care facilities, GlcN induced expression of KLF4, which regulated the maturation and maintenance of the ocular surface.
GlcN partially suppress the expression of TGF-β1-induced alpha-smooth muscle actin (α-SMA) and reduced collagen contraction capacity in health care facilities, showed a decrease in fibroblast-to-myofibroblast differentiation. This effect appears to be mediated through suppression of Smad2 phosphorylation and ERK-dependent signaling. KLF4 mRNA level increased by GlcN and decreased TGF-β1 and TGF-β1-induced expression of α-SMA mRNA was upregulated when KLF4 genes silenced. GlcN also appeared to stabilize KLF4 protein, reduce turnover in the cornea fibroblasts.
These findings explain the mechanism of a novel by which GlcN suppress TGF-β1-induced fibroblast-to-myofibroblast differentiation through upregulation of KLF4 expression. current strategies for treating corneal fibrosis ineffective. Raised levels of KLF4 through the use of GlcN may provide an effective alternative to ease the development and progression of corneal fibrosis.
Fibroblasts growth factor receptor 4 (FGFR 4 ) were detected by immunohistochemistry associated with postoperative residual disease in ovarian cancer.
Fibroblast Growth Factor Receptor 4 (FGFR4) proposed to hold prognostic significance in high-grade serous ovarian carcinoma (HGSOC). However, information about this comes from a large, representative patient panel is still missing, although such data would be necessary for compliance validation of FGFR4 as a prognostic marker or even a pharmacological target. 1063 cases of ovarian cancer were included in this study.
Immunohistochemistry (IHC) was performed using two different anti-FGFR4 specific antibody (HPA027273, sc-124) on the automated staining system. IHC data from two FGFR4 antibodies were available from 995 cases. FGFR4 immunostaining correlated with survival prognostic factors included using proportional hazards models uni and multivariate analyzes. FGFR4 positively associated with advanced FIGO stage, high grade and presence of residual disease.
Description: CRK, also known as p38, is a protein that in humans is encoded by the CRK gene. This gene is a member of an adapter protein family that binds to several tyrosine-phosphorylated proteins. It is mapped to 17p13.3. The protein participates in the Reelin signaling cascade downstream of DAB1. The product of this gene has several SH2 and SH3 domains (src-homology domains) and is involved in several signaling pathways, recruiting cytoplasmic proteins in the vicinity of tyrosine kinase through SH2-phosphotyrosine interaction. The N-terminal SH2 domain of Crk functions as a positive regulator of transformation whereas the C-terminal SH3 domain functions as a negative regulator of transformation. Two alternative transcripts encoding different isoforms with distinct biological activity have been described.
When the development of the free (PFS) of FGFR4 negative vs positive patients compared to patients scored as positive FGFR4 significantly shortened PFS compared with those who negatively stained. All associations FGFR4 and shortened PFS lost for multivariate testing. No significant association was found in the OS.
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