June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Suppression of TLR3-Inducible Gene Expression by EP3 in Conjunctival Epithelium
Author Affiliations & Notes
  • Mayumi Ueta
    Ophthalmology, Kyoto Prefectural Univ of Medicine, kyoto, Japan
    Research Center for Inflammation and Regenerative Medicine, Faculty of Life and Medical Sciences, Doshisha University, kyotanabe, Japan
  • Shuh Narumiya
    Department of Pharmacology and Faculty of Medicine, Kyoto University, kyoto, Japan
  • Shigeru Kinoshita
    Ophthalmology, Kyoto Prefectural Univ of Medicine, kyoto, Japan
  • Footnotes
    Commercial Relationships Mayumi Ueta, None; Shuh Narumiya, ONO Pharmaceuticals (F); Shigeru Kinoshita, Senju Pharmaceutical Co (P), Santen Pharmaceutical Co (P), Otsuka Pharmaceutical Co (C), Alcon (R), AMO (R), HOYA (R)
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 2080. doi:
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    • Get Citation

      Mayumi Ueta, Shuh Narumiya, Shigeru Kinoshita; Suppression of TLR3-Inducible Gene Expression by EP3 in Conjunctival Epithelium. Invest. Ophthalmol. Vis. Sci. 2013;54(15):2080.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: We previously reported that prostaglandin E receptor 3 (EP3) negatively regulates the eosinophilic infiltration of murine experimental allergic conjunctivitis induced by toll-like receptor 3 (TLR3), which causes reduced eosinophilic conjunctival inflammation in TLR3/EP3 double knockout (DKO) mice, despite the pronounced eosinophilic conjunctival inflammation in EP3 KO mice. It was also reported that EP3 was dominantly expressed in epithelial cells such as conjunctival epithelial cells, airway epithelial cells, and keratinocytes. In this study, to examine the effects of EP3 against TLR3-inducible gene expression in conjunctival epithelium, we performed gene expression analysis of polyinosinic:polycytidylic acid (polyI:C)-stimulated murine conjunctival epithelium in wild-type (WT)-, EP3-, and EP3/TLR3 DKO mice.

Methods: First, we examined the comprehensive effects of gene expression in polyI:C-stimulated murine conjunctival epithelium of WT mice using GeneChip® oligonucleotide microarrays. Then, to find the transcript regulated by EP3, we compared the gene expression of the transcripts, which were significantly and more than 3-fold upregulated, in polyI:C-stimulated conjunctival epithelium between WT and EP3 KO mice by quantitative reverse transcription polymerase chain reaction (RT-PCR).

Results: GeneChip® analysis showed that 131 transcripts were upregulated more than 3-fold and that 31 transcripts were upregulated more than 10-fold upon polyI:C stimulation of murine for 6 hours. Quantitative RT-PCR findings confirmed that 21 of 31 transcripts were significantly and more than 3 fold upregulated upon polyI:C stimulation in murine conjunctival epithelium. All of those 21 transcripts were found to be expressed in the polyI:C-stimulated conjunctival epithelium of EP3 KO mice significantly stronger than in that of WT mice. Moreover, mRNA expression of those 21 transcripts were confirmed to be significantly reduced in the polyI:C-stimulated conjunctival epithelium of EP3/TLR3 DKO mice than in that of EP3 KO mice.

Conclusions: EP3 suppressed the TLR3-inducible genes in polyI:C-stimulated conjunctival epithelium, which causes reduced gene expression in the conjunctival epithelium of TLR3/EP3 DKO mice, despite the pronounced gene expression in the conjunctival epithelium of EP3 KO mice.

Keywords: 474 conjunctiva • 482 cornea: epithelium  
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