July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
STAT3-mediated astrocyte reactivity within the optic nerve head preserves visual function.
Author Affiliations & Notes
  • Daniel Sun
    Ophthalmology, Massachusetts Eye & Ear Infirmary/Schepens Eye Research Institute, Boston, Massachusetts, United States
  • Sara Moore
    Ophthalmology, Massachusetts Eye & Ear Infirmary/Schepens Eye Research Institute, Boston, Massachusetts, United States
  • Tatjana C Jakobs
    Ophthalmology, Massachusetts Eye & Ear Infirmary/Schepens Eye Research Institute, Boston, Massachusetts, United States
  • Footnotes
    Commercial Relationships   Daniel Sun, None; Sara Moore, None; Tatjana Jakobs, Biogen (I), Merck (I), Qiagen (I), Santen Inc (R)
  • Footnotes
    Support  National Glaucoma Research a program of the BrightFocus Foundation, NIH R01 EY022092, NIH R01 EY019703, P30 EY003790
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 3737. doi:
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      Daniel Sun, Sara Moore, Tatjana C Jakobs; STAT3-mediated astrocyte reactivity within the optic nerve head preserves visual function.. Invest. Ophthalmol. Vis. Sci. 2018;59(9):3737.

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

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Abstract

Purpose : Reactive remodeling of astrocytes within the optic nerve head is observed in glaucoma and virtually all other optic nerve injuries. The mechanism and function of this reactivity is not well known. Is it beneficial or harmful for overall visual function?

Methods : We used a loss- and gain-of-function study to either attenuate or enhance astrocyte reactivity during experimental glaucoma and nerve crush, and then determined the effects on various histological and functional outcome measures. Reactivity was attenuated by conditional knockout of the transcription factor signal transducer and activator of transcription 3 (STAT3) from astrocytes using the Cre-loxP system under regulation of the mouse glial fibrillary acidic protein promoter. Reactivity was enhanced by knocking out suppressor of cytokine signaling 3 (SOCS3), the negative feedback molecule of STAT3. Visual function was assessed using the electroretinogram and optokinetic response.

Results : Following injury, STAT3 knockout mice displayed attenuated astrocyte hypertrophy and reactive remodeling, compared to controls. These changes were associated with significantly increased loss of ganglion cells and visual function over a 30-day period. In contrast, SOCS3 knockout mice showed improved survival of ganglion cells and visual function.

Conclusions : The STAT3 signaling pathway is an important mediator of various aspects of the reactive phenotype. Reactive astrocytes have a protective role early in glaucoma, preserving visual function.

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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