Abstract
Purpose To investigate whether retinal neuroinflammatory response was affected by aging in a rat model of acute glaucoma. Methods Young adult and aged rats were randomly assigned into normal control, 45 mmHg, 60 mmHg, and 90 mmHg groups. Intraocular pressure (IOP) of rats was acutely elevated to 45 mmHg, 60 mmHg, and 90 mmHg, respectively. Three days after high IOP treatment, loss of retinal ganglion cells (RGCs), formation of proinflammatory microglia/macrophages and neurotoxic astrocytes, and deposition of complement C3 in the retina were detected by immunofluorescence. ELISA was used to assess the protein levels of proinflammatory cytokines TNF and IL-1β in the retina. Results Compared with young adult retinae, (1) loss of RGCs was more severe in aged retinae under the same IOP treatment, (2) microglia/macrophages were more prone to adopt proinflammatory phenotype in aged retinae in response to elevated IOP, (3) high IOP treatment induced astrogliosis, formation of neurotoxic astrocytes, and deposition of complement C3 more easily in aged retinae, and (4) aged retinae induced higher levels of proinflammatory cytokines TNF and IL-1β under the same IOP treatment. Conclusion Our data indicated that aging affects the degree of retinal neuroinflammatory response initiated by ocular hypertension, which may contribute to the age-related susceptibility of RGCs to elevated IOP.
Highlights
Glaucoma is an age-related neurodegenerative disease and the leading cause of irreversible blindness worldwide [1]
retinal ganglion cells (RGCs) loss was more evident in aged retinae than young adult retinae at each intraocular pressure (IOP) treatment (Figures 1(q) and 1(r))
These results were consistent with our previous data [9], indicating that aged retinae are more vulnerable to increased IOP compared to young adult retinae
Summary
Glaucoma is an age-related neurodegenerative disease and the leading cause of irreversible blindness worldwide [1]. It is marked by the degeneration of retinal ganglion cell (RGC) axons, soma, and synapses [2]. Clinical studies have clearly established that increased intraocular pressure (IOP) is the major risk factor in glaucoma [3]. Therapeutic strategy for all types of glaucoma is limited to the reduction of elevated IOP, which does not completely stop the progression of glaucomatous neurodegeneration and visual field defects [4]. Besides IOP, age is another main risk factor of glaucoma [5, 6]. A body of studies has demonstrated that the prevalence of glaucoma increases markedly with advancing age across all populations [1, 7, 8]
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