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DSpace at SUNY >
SUNY College of Optometry >
SUNY Optometry Doctoral Dissertation Collection >
Please use this identifier to cite or link to this item:
http://hdl.handle.net/1951/41605
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| Title: | Roles of Calcium Signaling and Protein Kinase C Activation in Mediating Receptor Control of Corneal Epithelial Renewal |
| Authors: | Zhang, Fan |
| Keywords: | corneal epithelium calcium signaling epidermal growth factor |
| Issue Date: | 26-Jun-2007 |
| Abstract: | Epidermal growth factor, EGF, is one of the essential growth factors that stimulates injury-induced corneal epithelial healing rates. Cell signaling contributors mediating this response include capacitative calcium entry (CCE) activation and protein kinase C (PKC) isoform stimulation. This study shows in human corneal epithelial cells, HCEC, that CCE is preferentially activated by the PKC isoforms and . Moreover such activation requires increases in plasma membrane Ca2+ influx through store-operated channels. Therefore, EGF-induced stimulation of cell proliferation and migration may depend on unique effects mediated by six different PKC isoforms identified in HCEC. TRPV1 is a vanilloid subtype of the transient receptor potential protein superfamily. This isoform is a subunit of a non-selective cation channel mediating downstream responses to heat, low pH, or noxious stimuli. TRPV1 expression has been recently described in some epithelial tissues and induces proinflammatory cytokine release through mitogen-activated protein kinase (MAPK) superfamily stimulation. This study describes in HCEC the signaling pathways mediating TRPV1-induced increases in proinflammatory cytokine release. It suggests that epithelial TRPV1 receptor activation by noxious stimuli contributes in-vivo to mounting proinflammatory reactions. |
| URI: | http://hdl.handle.net/1951/41605 |
| Appears in Collections: | SUNY Optometry Doctoral Dissertation Collection |
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