September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
NOX2 induces photoreceptor apoptosis through endoplasmic reticulum stress pathway in a rat model of retinal detachment
Author Affiliations & Notes
  • Hong Zhu
    Opthalmology, Shanghai First People's Hospital, Shanghai, China
  • Quan Yan
    Opthalmology, Shanghai First People's Hospital, Shanghai, China
  • Fenghua Wang
    Opthalmology, Shanghai First People's Hospital, Shanghai, China
  • Xueting Luo
    Opthalmology, Shanghai First People's Hospital, Shanghai, China
  • Xiaodong Sun
    Opthalmology, Shanghai First People's Hospital, Shanghai, China
  • Footnotes
    Commercial Relationships   Hong Zhu, None; Quan Yan, None; Fenghua Wang, None; Xueting Luo, None; Xiaodong Sun, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 5375. doi:
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      Hong Zhu, Quan Yan, Fenghua Wang, Xueting Luo, Xiaodong Sun; NOX2 induces photoreceptor apoptosis through endoplasmic reticulum stress pathway in a rat model of retinal detachment. Invest. Ophthalmol. Vis. Sci. 2016;57(12):5375.

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

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Abstract

Purpose : To investigate the expression of NOX2, a NADPH oxidase, and its regulation on endoplasmic reticulum stress (ERS)-mediated apoptosis and photoreceptor damage using a rat model of retinal detachment (RD).

Methods : Animal model of RD was created in Brown Norway rats by subretinal injection of 1% sodium hyaluronate. Lentivirus NOX2 shRNA (LV-NOX2-sh) was constructed to inhibit NOX2 expression in vivo. The rats were randomly divided into four groups: normal control group (non-detachment), RD control group, negative control group (vehicle+RD) and LV-NOX2-sh+RD group. Expression of NOX2 and biomarkers of ERS pathway (CHOP, TRB3 and Caspase-12) were detected using quantitative real-time PCR and western blotting on day 1, 3, 5 and 7 after RD in each group. Non-detachment animals served as control. TdT-mediated fluorescein-16-dUTP nick-end labeling (TUNEL) assay was used to stain the apoptosis cells in histological sections. Retinal outer nuclear layer (ONL) thickness was measured to assess retina damage in each group.

Results : NOX2 expression was significantly increased after RD. CHOP and TRB3 were over-expressed in RD control group. In LV-NOX2-sh group, the expression of NOX2 was notably inhibited in vivo. And the expressions of CHOP and TRB3 were decreased compared with those RD rats and vehicle+RD rats at the same time points. The ratio of TUNEL-positive photoreceptors in LV-NOX2-sh+RD group was significantly reduced accompany with less expression of Caspase-12. Meanwhile, the ONL thickness in LV-NOX2-sh+RD group was thicker than that both in RD group and vehicle+RD group.

Conclusions : NOX2 expression is up-regulated in retinas and induces ERS pathway after RD. Inhibition of NOX2 protects photoreceptors through ERS-mediated apoptosis pathway in RD rat model. NOX2 may be a crucial regulatory molecule in ERS-mediated photoreceptor apoptosis after RD.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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