June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
The expression of prostaglandin E2 receptor 3 in the eyelid epidermis of patients with Stevens-Johnson syndrome/toxic epidermal necrolysis
Author Affiliations & Notes
  • Hiroki Mieno
    Kyoto Prefectural University of Medicine, Kyoto, Japan
  • Mayumi Ueta
    Kyoto Prefectural University of Medicine, Kyoto, Japan
  • Keiko Yamada
    Kyoto Prefectural University of Medicine, Kyoto, Japan
  • Yukito Yamanaka
    Kyoto Prefectural University of Medicine, Kyoto, Japan
  • Tomomichi Nakayama
    Kyoto Prefectural University of Medicine, Kyoto, Japan
  • Akihide Watanabe
    Kyoto Prefectural University of Medicine, Kyoto, Japan
  • Shigeru Kinoshita
    Kyoto Prefectural University of Medicine, Kyoto, Japan
  • Chie Sotozono
    Kyoto Prefectural University of Medicine, Kyoto, Japan
  • Footnotes
    Commercial Relationships   Hiroki Mieno, None; Mayumi Ueta, None; Keiko Yamada, None; Yukito Yamanaka, None; Tomomichi Nakayama, None; Akihide Watanabe, None; Shigeru Kinoshita, None; Chie Sotozono, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 3945. doi:
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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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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose :
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.

Methods :
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.

Results : DAB immunohistochemical staining revealed EP3 expression in the epidermis in all samples, including those of the SJS/TEN patients.

Conclusions : 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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