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Yuka Okada, Kumi Shirai, Masayasu Miyajima, Shizuya Saika; Favorable effects of loss of TRPM2 on the inflammation and scarring in an alkali-burned cornea in mice. Invest. Ophthalmol. Vis. Sci. 2013;54(15):3906.
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To determine if transient receptor potential melastatin 2 (TRPM2) gene ablation affects inflammation and scarring severity in a healing, alkali-burned, mouse cornea. TRPM2 is one of the TRP family cation channels and is reportedly important in inflammatory processes.
Immunohistochemistry probed for TRPM2 protein expression in mice corneas. Three μL of 1 N NaOH were applied under general anesthesia to the right eye of 6-8 week old TRPM2-null (KO) (n=44) or wild-type (WT) (n=44) mice to produce an ocular surface alkali burn. The eyes were processed for histology, immunohistochemistry or real time RT-PCR. Ocular fibroblasts from postnatal day 1 WT and KO mouse eyes were used to study the role of TRPM2 for pro-inflammatory gene expression.
TRPM2 protein was detected in uninjured corneal epithelium. Stroma of the KO healing corneas was less opaque as compared with those of WT mice at 5 to 20 days post-alkali burn. HE histological staining indicated more marked inflammation in the thickened stroma in the cornea of WT mice. Immunohistochemical and real time RT-PCR examinations show less appearance of myofibroblasts and less invasion of both leukocytes and macrophages in the cornea of KO mice after alkali burn. TRPM2 gene ablation suppressed mRNA expression of IL-6 and TGFb1 in cultured KO ocular fibroblasts. Exogenous TGFb1 up-regulated αSMA mRNA expression more prominently in WT cells than in KO cells.
The loss of TRPM2 improved outcome of the corneal wound healing response against an alkali exposure with suppression of inflammation and scarring.
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