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Oscar Manouchehrian, Karin M M Arner, Tomas Deierborg, Linnea T Taylor; Who let the dogs out?: Detrimental role of Galectin-3 in hypoperfusion-induced retinal degeneration. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):33.
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Retinal ischemia results in a progressive degeneration of neurons and a pathological activation of glial cells, resulting in vision loss. In the brain, progressive damage asfter ischemic insult has been correlated to neuroinflammatory processes involving microglia. Galectin-3 has been shown to mediate microglial responses to ischemic injury in the brain. Therefore, we wanted to explore the contribution of Galectin-3 (Gal-3) to hypoperfusion-induced retinal degeneration in mice.
Gal-3 knockout (Gal-3 KO) and WT C57BL/6 mice were subjected to chronic cerebral hypoperfusion by bilateral narrowing of the common carotid arteries using metal coils. Sham operated mice served as controls. After 17 weeks, the mice were sacrificed and the eyes were analyzed for retinal architecture, neuronal cell survival and glial reactivity using morphological staining and immunohistochemistry.
Hypoperfusion caused a strong increase in Gal-3 expression and microglial activation in WT mice, coupled with severe degenerative damage to all retinal neuronal subtypes, remodeling of the retinal lamination and Müller cell gliosis. In contrast, hypoperfused Gal-3 KO mice displayed a retained laminar architecture, a significant preservation of photoreceptors and ganglion cells neurons and an attenuation of microglial and Müller cell activation.
Gal-3 expression after ischemic insult mediates Müller cell and microglial activation, and results in significant retinal degenerative damage. These results for the first time show a link between neuroinflammation and reactive gliosis. Gal-3 is thereby a potential target for treatment and prevention of hypoperfusion-induced retinal degeneration, and a strong candidate for further research as a factor behind retinal degenerative disease.
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