April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
The Role of Tnf in Photoreceptor Degeneration After Retinal Detachment; Suppression With Dexamethasone Treatment
Author Affiliations & Notes
  • T. Nakazawa
    Ophthalmology, Tohoku Univ Graduate Sch of Med, Sendai, Japan
  • M. Ryu
    Ophthalmology, Tohoku Univ Graduate Sch of Med, Sendai, Japan
  • T. Hisatomi
    Angiogenesis,
    Massachusetts Eye & Ear Infirmary, Boston, Massachusetts
  • K. Noda
    Angiogenesis,
    Massachusetts Eye & Ear Infirmary, Boston, Massachusetts
  • S. Nakao
    Angiogenesis,
    Massachusetts Eye & Ear Infirmary, Boston, Massachusetts
  • M. Kayama
    Angiogenesis,
    Massachusetts Eye & Ear Infirmary, Boston, Massachusetts
  • A. Hafezi-Moghadam
    Angiogenesis,
    Massachusetts Eye & Ear Infirmary, Boston, Massachusetts
  • D. Vavvas
    Ophthalmology,
    Massachusetts Eye & Ear Infirmary, Boston, Massachusetts
  • K. Nishida
    Ophthalmology, Tohoku Univ Graduate Sch of Med, Sendai, Japan
  • J. W. Miller
    Ophthalmology,
    Massachusetts Eye & Ear Infirmary, Boston, Massachusetts
  • Footnotes
    Commercial Relationships  T. Nakazawa, None; M. Ryu, None; T. Hisatomi, None; K. Noda, None; S. Nakao, None; M. Kayama, None; A. Hafezi-Moghadam, None; D. Vavvas, None; K. Nishida, None; J.W. Miller, None.
  • Footnotes
    Support  MESCJ21659395
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 3718. doi:
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      T. Nakazawa, M. Ryu, T. Hisatomi, K. Noda, S. Nakao, M. Kayama, A. Hafezi-Moghadam, D. Vavvas, K. Nishida, J. W. Miller; The Role of Tnf in Photoreceptor Degeneration After Retinal Detachment; Suppression With Dexamethasone Treatment. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3718.

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

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Abstract

Purpose: : Photoreceptor degeneration is a major cause of visual loss in various retinal diseases. In this study, we investigated the role of anti-inflammatory treatment with dexamethasone (DEX) in retinal detachment (RD)-induced photoreceptor degeneration.

Methods: : RD was caused by subretinal injection of hyaluronaic acid. Photoreceptor degeneration was assessed by counting the TdT-dUTP terminal nick-end labeling (TUNEL)-positive cells and by measuring the outer nuclear layer thickness after RD. To understand the role of anti-inflammatory treatment, DEX (1mg/kg, IP) or nano particle of poly (γ-glutamic acid) with DEX (NP-DEX, 0.8 mg/ul, subretinally) was injected just after RD. As the target of anti-inflammatory treatment, the expression of TNFα with or without DEX was examined by real-time PCR and RD was performed in mice deficient in TNFα or its receptors (TNFRI, TNFRII, TNFRI&II).

Results: : Treatment with DEX (p=0.0005) or NP-DEX (p=0.0065) significantly suppressed RD-induced photoreceptor degeneration and the expression of TNFα. RD-induced photoreceptor degeneration was significantly suppressed in mice deficient for TNFα (p<0.0001), TNFRII (p=0.001), or TNFRI&II (p<0.0001). However, lack of TNFRI did not protect from RD-induced photoreceptor degeneration (p=0.06).

Conclusions: : Anti-inflammatory treatment with DEX had a neuroprotective effect against RD-induced photoreceptor degeneration. TNFα plays a critical role in RD-induced photoreceptor degeneration. This pathway may become an important target in the prevention of photoreceptor degeneration.

Keywords: apoptosis/cell death • neuroprotection • inflammation 
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