Interleukin-6 Protects Retinal Ganglion Cells from Pressure-Induced Death

Sappington, Rebecca M.; Chan, Matilda F.; Calkins, David J.

doi:10.1167/iovs.05-1407

Cited by 142 publications

(177 citation statements)

References 77 publications

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“…Rises in IL-6 suppress pro-apoptotic signalling pathways and cell death. 45 Therefore, provided strategies can be devised to selectively induce increases in microglial TRPV1 channels expression, TRPV1 channels may be a potential drug target in managing pressure-induced retinal ganglion cell loss in glaucoma.…”

Section: Roles Of Trp Channels In Glaucomamentioning

confidence: 99%

Transient Receptor Potential (TRP) Channels in the Eye

Pan¹,

Capó-Aponte²,

Reinach³

2012

Advances in Ophthalmology

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Section: Roles Of Trp Channels In Glaucomamentioning

confidence: 99%

Transient Receptor Potential (TRP) Channels in the Eye

Pan¹,

Capó-Aponte²,

Reinach³

2012

Advances in Ophthalmology

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“…Previous research indicates that inflammatory responses in the retina, including glial cell activation and production of inflammatory cytokines [5][6][7][8][9][10][11][12][13][14][15][16][17][18], play a role in glaucomatous degeneration of RGCs. These inflammatory responses can be either detrimental or neuroprotective for RGCs challenged by glaucomatous stressors.…”

Section: Introductionmentioning

confidence: 99%

Stressor-dependent Alterations in Glycoprotein 130: Implications for Glial Cell Reactivity, Cytokine Signaling and Ganglion Cell Health in Glaucoma

Echevarria

et al. 2013

J Clin Exp Ophthalmol

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Objective: The interleukin-6 (IL-6) family of cytokines is associated with retinal ganglion cell (RGC) survival and glial reactivity in glaucoma. The purpose of this study was to evaluate glaucoma-related changes in glycoprotein-130 (gp130), the common signal transducer of the IL-6 family of cytokines, as they relate to RGC health, glial reactivity and expression of IL-6 cytokine family members. Methods:For all experiments, we examined healthy retina (young C57), aged retina (aged C57), retina predisposed to glaucoma (young DBA/2) and retina with IOP-induced glaucoma (aged DBA/2). We determined retinal gene expression of gp130 and IL-6 family members, using quantitative PCR, and protein expression of gp130, using multiplex ELISA. For protein localization and cell-specific expression, we performed co-immunolabeling for gp130 and cell type-specific markers. We used quantitative microscopy to measure layer-specific expression of gp130 and its relationships to astrocyte and Müller glia reactivity and RGC axonal transport, as determined by uptake and transport of cholera toxin β-subunit (CTB).Results: Gene expression of gp130 was elevated with all glaucoma-related stressors, but only normal aging increased protein levels. In healthy retina, gp130 localized primarily to the inner retina, where it was expressed by astrocytes, Müller cells and RGCs. Layer-specific analysis of gp130 expression revealed increased expression in aging retina and decreased expression in glaucomatous retina that was eccentricity-dependent. These glaucoma-related changes in gp130 expression correlated with the level of GFAP and glutamine synthetase expression, as well as axonal transport in RGCs. The relationships between gp130, glial reactivity and RGC health could impact signaling by many IL-6 family cytokines, which exhibited overall increased expression in a stressor-dependent manner.Conclusions: Glaucoma-related stressors, including normal aging, glaucoma predisposition and IOP-induced glaucoma, differentially alter expression of gp130 and these alterations have direct implications for astrocyte and Müller glia reactivity, RGC health and cytokine signaling.

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“…Elevated pressure is a significant risk factor (2,3). Although the role of glial cells in glaucomatous retinae remains under debate, certain research has found that the expression of various genes by Müller cells can be altered in glaucomatous models, including the glial fibrillary acidic protein (GFAP), glutamine synthetase (GS) and nestin (1,(4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

“…T75 culture flasks, equipped with manometers, were placed in incubators and maintained at 37˚C, as the pressure mechanism, as described in detail in our previous study (3). A mixture of 95% air and 5% CO 2 was pumped into the flasks to obtain the pressure (2). To determine the short-term effects of elevated pressure on the Müller cells, we exposed our cultures to a wide range of pressures (20,40, 60 and 80 mmHg).…”

Section: Introductionmentioning

confidence: 99%