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Yuka Nidegawa, Takayoshi Sumioka, Yuka Okada, Masayasu Miyajima, Peter S Reinach, Shizuya Saika; Impaired wound healing in corneal stroma of a TRPV1-deficient mouse model.. Invest. Ophthalmol. Vis. Sci. 2014;55(13):4692.
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© ARVO (1962-2015); The Authors (2016-present)
We determined in mice if loss of transient receptor potential protein vanilloid 1 isoform (TRPV1) affects the wound healing in corneal stroma in response to an incision-injury in mice. TRPV1 is a nonselective cation channel expressed in corneal epithelium, keratocytes and sensory nerves.
TRPV1-null (KO) mice (n =106) or C57BL/6 wild-type (WT) mice (n= 106) were used. A full-thickness penetrating incision injury (1.8 mm in length) was produced in the central cornea by using a micro surgical blade. The eyes were processed for histology, immunohistochemistry or real-time RT-PCR for expression of wound healing-related components.
Healing (closure) of incision injury in corneal stroma was delayed in a KO mouse as compared with a WT mouse. Immunohistochemical examination showed less population of α-smooth muscle actin-labeled myofibroblasts. The loss of TRPV1 suppressed mRNA expression of collagen Ia1.
Loss of TRPV1 impaired wound healing in corneal stroma in response to an incision-injury in mice. The mechanism of action might include suppression of fibrotic reaction and macropahge invasion in the injured corneal stroma by lacking TRPV1.
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