Insulin-like Growth Factor-1 Induces Migration and Expression of Laminin-5 in Cultured Human Corneal Epithelial Cells

2006 ◽  
Vol 47 (3) ◽  
pp. 873 ◽  
Author(s):  
Hyung Keun Lee ◽  
Joon H. Lee ◽  
Min Kim ◽  
Yoshinobu Kariya ◽  
Kaoru Miyazaki ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Insulin Like Growth Factor ◽  
Corneal Epithelial Cells ◽  
Laminin 5 ◽  
Corneal Epithelial ◽  
Human Corneal Epithelial Cells

scholarly journals Nerve growth factor inhibits TLR3-induced inflammatory cascades in human corneal epithelial cells

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Huiyu Chen ◽  
Jing Zhang ◽  
Yiqin Dai ◽  
Jianjiang Xu
Keyword(s):  
Nerve Growth Factor ◽  
Herpes Simplex ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Proinflammatory Cytokines ◽  
Corneal Epithelial Cells ◽  
Nerve Growth ◽  
Corneal Epithelial ◽  
Human Corneal Epithelial Cells ◽  
Tlr3 Activation

Abstract Background In herpes simplex epithelial keratitis, excessive TLR3-induced cellular responses after virus infection evoke inflammatory cascades that might be destructive to the host cornea. Nerve growth factor (NGF), a pluripotent neurotrophic factor with immune regulatory effect, was proved to be effective in Herpes simplex keratitis (HSK) treatment, although the detailed mechanisms remain unclear. This study aims to investigate the effects of NGF on modulating inflammatory responses triggered by TLR3 activation in human corneal epithelial cells (HCECs) in vitro. Methods HCECs were stimulated with TLR3 agonist, poly(I:C), in the absence or presence of NGF. Cell viability and cytotoxicity were measured by a CCK-8 assay and LDH release assay, respectively. The activation of NF-κB signaling pathway was examined using immunofluorescence staining and western blotting. Levels of proinflammatory cytokines were determined by ELISA or RT-qPCR. ROS generation and 8-OHdG positive cells were examined by a fluorometric analysis. Results It was shown that NGF significantly inhibited the generation of proinflammatory cytokines in HCECs triggered by TLR3 activation (P < 0.05), probably via suppressing NF-κB activation. NGF also impeded the upstream signal to initiate NF-κB activation by scavenging ROS by approximately 50% (P < 0.05). In addition, 8-OHdG positive cells were substantially attenuated by NGF treatment (P < 0.01). Conclusions Taken together, this study indicates that NGF could inhibit TLR3-induced inflammatory cascades in HCECs, suggesting NGF as a potential therapeutic agent for HSK.

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