July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
Mitochondrial Dysfunction in Photoreceptors after Retinal Detachment
Author Affiliations & Notes
  • Xueting Luo
    Ophthalmology, Shanghai General Hospital, Shanghai, China
  • Xiangjun She
    Ophthalmology, Shanghai General Hospital, Shanghai, China
  • Xinmin Lu
    Ophthalmology, Shanghai General Hospital, Shanghai, China
  • Xiaodong Sun
    Ophthalmology, Shanghai General Hospital, Shanghai, China
  • Footnotes
    Commercial Relationships   Xueting Luo, None; Xiangjun She, None; Xinmin Lu, None; Xiaodong Sun, None
  • Footnotes
    Support  National Science Fund for Distinguished Young Scholars (81425006), National Natural Science Foundation of China (81470640), Science and Technology Commission of Shanghai Municipality (16dz2251500, 16140900800), Shanghai Pujiang Program (16PJ1408500), Program for Eastern Young Scholar at Shanghai Institutions of Higher Learning (QD2016003), Translational Medicine Innovation Fund of Shanghai Jiao Tong University School of Medicine (15ZH4005)
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 967. doi:
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    • Get Citation

      Xueting Luo, Xiangjun She, Xinmin Lu, Xiaodong Sun; Mitochondrial Dysfunction in Photoreceptors after Retinal Detachment
      . Invest. Ophthalmol. Vis. Sci. 2018;59(9):967.

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

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Abstract

Purpose : To dissect the mechanism underlying photoreceptor degeneration after retinal detachment.

Methods : The vitreous from patients with retinal detachment was analyzed by quantitative metabolics. A rat model of retinal detachment and cultured photoreceptors subjected to oxidative stress were also employed to interrogate underlying molecular mechanisms.

Results : Key metabolites in the glycolytic pathway were dysregulated in the vitreous of patients with retinal detachment. In the animal models, We showed that retinal detachment activated dynamin-related protein 1 dependent mitochondrial fission, ROS release and apoptotic cascades. Pharmacological blockade or RNA interference of dynamin-related protein 1 activity preserved mitochondrial integrity, attenuated ROS production and rescued photoreceptors both in vivo and in vitro.

Conclusions : Our findings have identified mitochondrial fission as a critical ‘danger signal’ to photoreceptor degeneration and dynamin-related protein 1 as a promising therapeutic target for photoreceptor protection after retinal detachment.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.

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