ArticleInvestigative ophthalmology & visual science2025
Autophagy Regulates Müller Glial Cell Inflammatory Activation.
Article in Investigative ophthalmology & visual science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: We tested whether Müller cells utilize autophagy to support immune privilege in the eye. Methods: The essential autophagy gene Atg5 was deleted in retinal Müller cells. Inflammation was induced by intravitreal injection of lipopolysaccharide (LPS) that was monitored by hematoxylin and eosin (H&E) staining, immunofluorescent confocal microscopy, and flow cytometry. Single-cell RNA sequencing was performed on retinal Müller cells isolated from control and Atg5-deficient mice. Markers of Müller cell gliosis were assessed, and cytokine production in the eye was measured. Small interfering RNA knockdown techniques were used to examine LPS-induced inflammatory pathways in culture. Results: We observed increased and prolonged intraocular inflammation when Müller cells were autophagy (Atg5) deficient. Müller cell gliosis was significantly increased, and the retinae contained increased inflammatory mediators. Gene expression analysis revealed a heterogeneous response to LPS in Müller cells, revealing two states of activation. The normal retinae contained both basal and activated Müller cells, whereas the autophagy-deficient retinae contained only activated cells. Analysis of the gliosis markers glial fibrillary acidic protein (Gfap) and lipocalin-2 (Lcn2) confirmed this heterogeneity, as in control eyes basal and activated (gliotic) Müller glia were observed; however, with autophagy deficiency, all Müller cells were gliotic. Activated cells were largely indistinguishable between autophagy-sufficient and -deficient Müller cells. In cultured Müller cells, knockdown of Atg5 resulted in heightened mechanistic target of rapamycin (mTOR) activation, increased Gfap expression, and upregulated cytokine/chemokine production in response to LPS. Conclusions: Autophagy regulates the activation state of Müller cells in response to LPS. Thus, autophagy restrains cellular activation and inflammation, supporting immune privilege by preventing excessive and potentially destructive immune responses.
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