Sensory nerve supports epithelial stem cell function in healing of corneal epithelium in mice: the role of trigeminal nerve transient ... View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2018-11-09

AUTHORS

Yuka Okada, Takayoshi Sumioka, Kana Ichikawa, Hiromi Sano, Atsushi Nambu, Kenta Kobayashi, Kunitoshi Uchida, Yoshiro Suzuki, Makoto Tominaga, Peter Sol Reinach, Syu-ichi Hirai, James V. Jester, Masayasu Miyajima, Kumi Shirai, Hiroki Iwanishi, Winston Whei-Yang Kao, Chia-Yang Liu, Shizuya Saika

ABSTRACT

In order to understand the pathobiology of neurotrophic keratopathy, we established a mouse model by coagulating the first branch of the trigeminal nerve (V1 nerve). In our model, the sensory nerve in the central cornea disappeared and remaining fibers were sparse in the peripheral limbal region. Impaired corneal epithelial healing in the mouse model was associated with suppression of both cell proliferation and expression of stem cell markers in peripheral/limbal epithelium as well as a reduction of transient receptor potential vanilloid 4 (TRPV4) expression in tissue. TRPV4 gene knockout also suppressed epithelial repair in mouse cornea, although it did not seem to directly modulate migration of epithelium. In a co-culture experiment, TRPV4-introduced KO trigeminal ganglion upregulated nerve growth factor (NGF) in cultured corneal epithelial cells, but ganglion with a control vector did not. TRPV4 gene introduction into a damaged V1 nerve rescues the impairment of epithelial healing in association with partial recovery of the stem/progenitor cell markers and upregulation of cell proliferation and of NGF expression in the peripheral/limbal epithelium. Gene transfer of TRPV4 did not accelerate the regeneration of nerve fibers. Sensory nerve TRPV4 is critical to maintain stemness of peripheral/limbal basal cells, and is one of the major mechanisms of homeostasis maintenance of corneal epithelium. More... »

PAGES

1-21

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41374-018-0118-4

DOI

http://dx.doi.org/10.1038/s41374-018-0118-4

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1108043067

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30413814


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427 https://www.grid.ac/institutes/grid.275033.0 schema:alternateName Graduate University For Advanced Studies
428 schema:name Department of Physiological Sciences, SOKENDAI (The Graduate University for Advanced Studies), Okazaki, Japan
429 Division of Cell Signaling, National Institute for Physiological Sciences, Okazaki, Japan
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431 https://www.grid.ac/institutes/grid.411377.7 schema:alternateName Indiana University Bloomington
432 schema:name School of Optometry, Indiana University Bloomington, Bloomington, IN, USA
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434 https://www.grid.ac/institutes/grid.412857.d schema:alternateName Wakayama Medical University
435 schema:name Department of Ophthalmology, Wakayama Medical University School of Medicine, Wakayama, Japan
436 Educational Phyilosophy/Cell Biology, Wakayama Medical University School of Medicine, Wakayama, Japan
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438 https://www.grid.ac/institutes/grid.467811.d schema:alternateName National Institute for Physiological Sciences
439 schema:name Division of System Neurophysiology, National Institute for Physiological Sciences, Okazaki, Japan
440 Section of Viral Vector Development, National Institute for Physiological Sciences, Okazaki, Japan
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