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Takayoshi Sumioka, Yuka Okada, Peter S. Reinach, Norihito Fujita, Masayasu Miyajima, Shizuya Saika; Lacking Trpv1 Ion Channel Receptor Suppresses Cytokines And Substance P In An Epithelium-debrided Cornea In Mice. Invest. Ophthalmol. Vis. Sci. 2012;53(14):4746.
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To investigate the effects of lacking transient receptor potential cation channel subfamily V member 1 (TRPV1) receptor on expression of transforming growth factor β1 (TGFβ1), substance P and interleukin-6 (IL-6), all of which are involved in epithelial healing in cornea in mice. Healing of the epithelial defect was also assayed. Substance P is known to be expressed in sensory nerve fibers in cornea.
Corneal epithelial wounds were made in TRPV1 -/- (KO, n = 35) and wild type (WT) mice (n = 35) with 2mm trephine. Healing corneas were processed for total RNA extraction and real-time RT-PCR for TGFβ1, substance P and IL-6 at 6, 12 and 18 hrs post-debridement. Healing pattern of the epithelial defect was also evaluated by the measurement of the remaining defect and histological detection of BrdU-labeled epithelial cells.
Expression of mRNAs of Substance P and IL-6, but not TGFβ1, was significantly less in a KO cornea as compared with a WT cornea at 12 hrs. The loss of TRPV1 receptor impaired resurfacing of the defected corneal epithelium and also suppressed cell proliferation in healing epithelium 24 and 36 hours.
Lacking TRPV1 ion channel receptor suppressed mRNA expression of substance P and IL-6, as well as impaired healing of corneal epithelium in mice.
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