In vivo, the BALB/c mouse psoriasis model established by topical application of imiquimod (IMQ) was used to determine the role of FGF-7-specific antibody (F-9) in skin inflammation.
The aim of the present study was to evaluate the ability of HGF and KGF to influence VEGF and its receptor, kinase insert domain receptor (Flk‑1) in corneal injury and CNV in rats induced by ultraviolet radiation (UVR).
Western blot of lung tissue confirmed high expression of KGF and their target molecules (interleukin-6, protein kinase B, and B-cell lymphoma-2) in the Muse group.
Chemotherapy (P < .001) and baseline keratinocyte growth factor (P = .019) predicted acute esophagitis, but only chemotherapy remained significant after Bonferroni correction.
Higher percentages of stromal cells in FECD versus normal stained for αSMA (OR = 864.26, P < 0.001), brain-derived neurotrophic factor (BDNF, OR = 6.34, P = 0.005), fibroblast growth factor 7 (FGF-7, OR = 2.76, P = 0.011), FGF-9 (OR = 5.97, P < 0.001), receptor FGFR-3 (OR = 13.90, P = < 0.001), and serum amyloid A1 (OR = 3.45, P = 0.023).
Coadministration of KGF with IAV markedly accelerated the spread of viral infection from the airways to alveoli compared with challenge with IAV alone, based on spatial and temporal analyses of viral nucleoprotein staining of lung tissue sections and dissociated lung cells.
Our results indicated that the abnormal behavior of the cholesteatoma epithelium seems to be induced by the paracrine interaction between KGF and KGFR.
The purpose of this study was to investigate the potential influence of KGF and KGFR in increased epithelial-cell proliferation of chronic otitis media (COM) with cholesteatoma in contrast to COM without cholesteatoma (CSOM), particularly in the granulative form, and to compare the rate of proliferation activity of epithelial cells using the Ki-67 epithelial proliferation marker expression.
Keratinocyte growth factor for the treatment of the acute respiratory distress syndrome (KARE): a randomised, double-blind, placebo-controlled phase 2 trial.
To better define the temporal relationship between KGF administration and susceptibility to IAV infection in vivo, we administered KGF 120, 48, 24, and 0 h before intrapulmonary IAV challenge and assessed the percentages of proliferating and IAV-infected, alveolar type II (AECII) cells in dispersed lung cell populations.
In this study we tested the hypothesis that endogenous KGF plays a role in the maintenance of innate pulmonary defense against gram-negative bacterial infections.
We then used our well characterized urothelial carcinoma cohort to analyze FGF7 transcript and protein expression, and its clinicopathological significance.
An increased FGF7 transcript level was associated with higher pT stage in upper tract and bladder urothelial carcinoma (p = 0.003 and <0.001, respectively).
In the upper tract and bladder carcinoma groups FGF7 protein over expression was also significantly associated with advanced pT status (each p <0.001), lymph node metastasis (p = 0.002 and <0.001), high histological grade (p = 0.019 and <0.001), vascular invasion (each p <0.001), perineural invasion (p = 0.002 and 0.021) and frequent mitoses (p = 0.002 and 0.042, respectively).
In the upper tract and bladder carcinoma groups FGF7 protein over expression was also significantly associated with advanced pT status (each p <0.001), lymph node metastasis (p = 0.002 and <0.001), high histological grade (p = 0.019 and <0.001), vascular invasion (each p <0.001), perineural invasion (p = 0.002 and 0.021) and frequent mitoses (p = 0.002 and 0.042, respectively).