July 2019
Volume 60, Issue 9
Free
ARVO Annual Meeting Abstract  |   July 2019
Minocycline protects retinal ganglion cells and optic nerve structure in an immune mediated retina degeneration model
Author Affiliations & Notes
  • Andreas Smit
    Experimental Eye Research Institute, Ruhr University Bochum, Bochum, Germany
  • Pia Grotegut
    Experimental Eye Research Institute, Ruhr University Bochum, Bochum, Germany
  • Sandra Kuehn
    Experimental Eye Research Institute, Ruhr University Bochum, Bochum, Germany
  • Gesa Stute
    Experimental Eye Research Institute, Ruhr University Bochum, Bochum, Germany
  • Burkhard Dick
    Experimental Eye Research Institute, Ruhr University Bochum, Bochum, Germany
  • Stephanie C Joachim
    Experimental Eye Research Institute, Ruhr University Bochum, Bochum, Germany
  • Footnotes
    Commercial Relationships   Andreas Smit, None; Pia Grotegut, None; Sandra Kuehn, None; Gesa Stute, None; Burkhard Dick, None; Stephanie Joachim, None
  • Footnotes
    Support  Foundation: Ernst und Berta Grimmke Stiftung
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 3111. doi:
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      Andreas Smit, Pia Grotegut, Sandra Kuehn, Gesa Stute, Burkhard Dick, Stephanie C Joachim; Minocycline protects retinal ganglion cells and optic nerve structure in an immune mediated retina degeneration model. Invest. Ophthalmol. Vis. Sci. 2019;60(9):3111.

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

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Abstract

Purpose : Previous studies have shown that intraocular injection of S100B leads to glaucoma-like damage in a rodent model (Kuehn et al., 2018). Also, a microglial response was found in this model. The role of this microglial reaction in the degenerative processes remains unclear. Hence, we inhibited the microglial activity by systemic minocycline treatment.

Methods : Four groups were part of the study. Three groups received intraocular S100B injections whereas PBS served as a control. Two groups amongst the S100B groups received additional intraperitoneal injections of minocycline hydrochloride in two different doses (25 mg/kg BW=mino I and 13.5 mg/kg BW=mino II). Minocycline treatment started one day prior to intraocular injections and was continued daily for 14 days. At day 14 immunohistochemical analysis of retinal ganglion cells (Brn-3a) as well as apoptosis (cleaved caspase 3) followed. Additionally, the neurofilament (SMI-32) and microglia (Iba1/ED1) of the optic nerve (ON) were analyzed.

Results : A decrease in retinal ganglion cell (RGC) numbers was noted in the S100B group (30.3±1,7 cells/mm, p=0.02) compared to the PBS group (52.0±4.7 cells/mm). Also, an increase of apoptotic activity was observed in the S100B group (31.5±3.5%, p<0.001) in comparison to the control (7.3±3.9%). Minocycline groups showed apoptotic activity similar to the control group (mino I: 16.7±5.0%, p=0.4; mino II: 8.0±1.7%, p>0.9), as well as a tendency to RGC protection (mino I: 40.4±5.3 cells/mm, p=0.4; mino II: 40.1±3.2 cells/mm, p=0.4). S100B injection lead to an increase of optic nerve neurofilament score (1.3±0.1, p=0.016) indicating loss of structural integrity compared to control group (0.8±0.1). In minocycline treated groups, a dose-dependent protection of the nerve structure occurred (mino I: 1.1±0.2, p=0.448; mino II: 0.9±0.3, p<0.05). Furthermore, a significant increase in microglial cell count has been shown in the S100B group (167.9±22.9%, p<0.001) compared to the control (108.3±16.4%) that could not be seen in the minocycline groups (mino I: 95.4±15.1%, p=0.68; mino II=100.4±10.3%, p=0.9).

Conclusions : An inhibition of the microglial response through minocycline has a protective effect on the retinal and optic nerve structure. However, the damage has not been prevented completely, thus the microglial response only seems to have a partial role in the degenerative process.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.

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