July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
Regulation of microglia activation by CSFs drives neurodegeneration in glaucoma
Author Affiliations & Notes
  • Min Ji
    Opthalmology Institute, Affiliated hospital of Nantong University, Nantong, China
  • Kin-Sang Cho
    Schepens Eye Research Institute, Boston, Massachusetts, United States
  • Huaijin Guan
    Opthalmology Institute, Affiliated hospital of Nantong University, Nantong, China
  • Dong Feng Chen
    Schepens Eye Research Institute, Boston, Massachusetts, United States
  • Footnotes
    Commercial Relationships   Min Ji, None; Kin-Sang Cho, None; Huaijin Guan, None; Dong Chen, None
  • Footnotes
    Support  NIH/NEI R01EY025259, P30EY03790, and Lion’s Foundation grant, National Natural science Foundation of China(81670852)
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 2014. doi:
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      Min Ji, Kin-Sang Cho, Huaijin Guan, Dong Feng Chen; Regulation of microglia activation by CSFs drives neurodegeneration in glaucoma. Invest. Ophthalmol. Vis. Sci. 2018;59(9):2014.

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

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Abstract

Purpose : Recent studies in our lab showed that mice raised in the absence of microflora (germ-free mice) do not develop retinal ganglion cells (RGC) damage following elevation of intraocular pressure (IOP). Moreover, we noted that the expression of colony stimulating factor 1 (CSF1) was downregulated, while CSF2 was upregulated in germ-free mice. We proposed that CSF1 and CSF2 play an opposing role mediating RGC loss in glaucoma. Herein, we examined the expression and involvement of CSF1 and CSF2 in a mouse model of glaucoma.

Methods : Microbeads (MB) was injected into the anterior chamber of adult B6 mice to induce high IOP. The expression of CSF1/2 and their receptors was examined by immunostaining and quantitative polymerase chain reaction (qPCR) at different time points after MB injection. CSF2 and/or neutralizing antibody of CSF1 were adminstered intravitreally to mice with high IOP. Anti-brn3a staining was used to label RGC in the whole-mount retina.

Results : In line with our hypothesis, the expression of CSF1 was upregulated while CSF2 was downregulated in the retina 2 weeks after MB injection. Our data also showed that Administration of either CSF2 or neutralizing antibody of CSF1 attenuated glaucomatous RGC loss compared to saline-treated control mice. CSF1 receptor was found to associate with microglia and RGCs while CSF2 receptor was expressed by Müller cells and RGCs.

Conclusions : CSF1 and CSF2 play opposing roles on microglia and Müller cells activation under elevated IOP that drive glaucomatous RGC degeneration. This finding points to novel therapeutic strategies for preventing RGC and vision loss in glaucoma.

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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