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Hiroki Mieno, Mayumi Ueta, Keiko Yamada, Yukito Yamanaka, Tomomichi Nakayama, Akihide Watanabe, Shigeru Kinoshita, Chie Sotozono; The expression of prostaglandin E2 receptor 3 in the eyelid epidermis of patients with Stevens-Johnson syndrome/toxic epidermal necrolysis. Invest. Ophthalmol. Vis. Sci. 2017;58(8):3945.
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We previously performed a genome-wide association study of Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) patients and reported the association between SJS/TEN and the prostaglandin E receptor 3 (PTGER3) gene. Prostaglandin E2 receptor 3 (EP3) is encoded by the PTGER3 gene. We also reported that prostaglandin E2-EP3 signaling inhibits keratinocyte activation and exerts an anti-inflammatory effect in a murine contact dermatitis model. The purpose of this present study was to investigate the expression of EP3 in the eyelid epidermis of patients with SJS/TEN.
We obtained eyelid samples from SJS/TEN patients (n=3) and patients without SJS/TEN (n=3) who were undergoing surgery to treat trichiasis and compared the expression of EP3 in the epidermis of those samples between those two groups of patients. Immunostaining was performed via the 3, 3'-diaminobenzidine (DAB) immunological staining method.
DAB immunohistochemical staining revealed EP3 expression in the epidermis in all samples, including those of the SJS/TEN patients.
In this study, we found that the expression of EP3 in the eyelid epidermis of SJS/TEN patients was not downregulated. We previously reported that EP3 was markedly downregulated in the conjunctival epithelium of SJS/TEN patients. This finding possibly suggests that the expression of EP3 in the epidermis does not contribute to the ocular inflammation in the chronic stage of SJS/TEN.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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