June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Pentraxin3 in proliferative diabetic retinopathy
Author Affiliations & Notes
  • Kazunori Tamaki
    Department of ophthalmology, Juntendo University Urayasu Hospital, Urayasu city, Chiba, Japan
  • Ayumi Usui
    Department of ophthalmology, Juntendo University Urayasu Hospital, Urayasu city, Chiba, Japan
  • Nobuyuki Ebihara
    Department of ophthalmology, Juntendo University Urayasu Hospital, Urayasu city, Chiba, Japan
  • Footnotes
    Commercial Relationships   Kazunori Tamaki, None; Ayumi Usui, None; Nobuyuki Ebihara, None
  • Footnotes
    Support  none
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 5216. doi:
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      Kazunori Tamaki, Ayumi Usui, Nobuyuki Ebihara; Pentraxin3 in proliferative diabetic retinopathy
      . Invest. Ophthalmol. Vis. Sci. 2017;58(8):5216.

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

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Abstract

Purpose : Recently, there are many studies suggesting that inflammatory cytokines are involved in the pathogenesis of diabetic retinopathy. Pentraxin3 (PTX3) is one of the long pentraxins and is an acute phase protein that has emerged as a serological marker reflecting tissue inflammation/damage. PTX3 is produced mainly by vascular endothelial cells, fibroblasts, and resident cells in tissues. PTX3 is a soluble pattern recognition receptor that binds with high affinity and selectivity to fibroblast growth factor-2 (FGF2), thus inhibiting its pro-angiogenic activity. The purpose of this study is to investigate the role of PTX3 in the pathogenesis of proliferative diabetic retinopathy (PDR).

Methods : This study was performed in accordance with the Declaration of Helsinki and the ethics committees of our Hospital. Vitreous samples were collected from 19 eyes of 18 patients with PDR and 13 eyes of 13 patients with macular hole (MH) as controls. The concentrations of PTX3 were determined by enzyme-linked immunosorbent assay (ELISA). In human retinal microvascular endothelial (HRME) cells, we analyzed PTX3 production in the presence or absence of inflammatory cytokines, such as TNF-αand IL-1β using ELISA. Wound healing assay was performed on HRME cells stimulated with FGF2 as the functional assay of PTX3.

Results : The PTX3 concentrations were significantly higher in vitreous fluid samples from PDR patients than in MH patients (901.1±421.8 pg/ml versus 280.8±178.4 pg/ml, p<0.05). Production of PTX3 was dose-dependently induced by TNF-αand IL-1βin HRME cells. PTX3 inhibited HRME cells migration induced by FGF2 as assessed by a wound healing assay.

Conclusions : These findings may indicate that PTX3 is involved in the pathogenesis of PDR.

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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