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Yuka Okada, Peter S Reinach, Masayasu Miyajima, Shizuya Saika; Effects of loss of TRPV4 function on corneal epithelial wound healing in mice.. Invest. Ophthalmol. Vis. Sci. 2016;57(12):1253.
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© 2017 Association for Research in Vision and Ophthalmology.
To determine if transient receptor potential vanilloid 4 (TRPV4), TRPV1-related component, contributes to epithelial wound healing in a mouse cornea. Growth factor expression pattern was also evaluated. TRP family consists of groups of TRPV, ankyrin 1 (TRPA1) or melastatin (TRPM). We previously reported the involvement of TRPV1 and TRPA1 in corneal epithelial wound healing in mice (IOVS 2014, ARVO 2015).
Imunohistochemistry was carried out to examine the expression opattern of TRPV4 in mouse cornea. Time dependent closure of a 2.0 mm diameter central corneal epithelial debridement was monitored in the right eyes of C57BL/6 (wild type, WT, n =61) and TRPV4-null (KO, n =61) mice for up to 36 h using fluorescein green staining. BrdU-labeling in WT and KO mice evaluated proliferative activity during healing. RT-PCR analyzed interleukin 6 (IL-6), substance P (SP) calcitonin gene-related peptide (CGRP), nerve growth factor (NGF) and transforming growth factor b1 (TGFb1) gene expression levels.
TRPV4 was detected in the basal cells of the corneal epithelium. The open wound area in the TRPV4 KO mice at 18 and 24 hr was 1.6-fold and 7.34-fold bigger than in the WT counterpart, respectively. BrdU-labeled cells were fewer in the KO healing epithelium than in the WT counterpart at 24 and 36 hr (p<0.05). Increases in CGRP, NGF and TGFb1 gene expression were smaller than those in the WT counterpart (p<0.05) whereas increases in IL-6 and SP were unaffected by the loss of TRPV4 function.
TRPV4 mediated signaling contributes to increases in CGRP, NGF and TGFb1 gene expression and repair of a corneal epithelial debridement in mice.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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