Lipoxin B4 Mitigates TRPV4-Activated Muller Cell Gliosis During Ocular Hypertension.

ABSTRACT:

Purpose

Müller glia play dual roles in glaucoma, contributing to retinal homeostasis and neuroinflammation; activation by elevated intraocular pressure through mechanosensitive transient receptor potential vanilloid 4 (TRPV4) promotes a reactive state that drives retinal ganglion cell loss. Lipoxin B4 (LXB4), an endogenous lipid mediator produced by retinal astrocytes, suppresses glial reactivity and protects retinal ganglion cells. This study investigated whether LXB4 modulates TRPV4-driven Müller glial activation and whether Müller glia contribute to the lipoxin pathway.

Methods

Ocular hypertension was induced in mice via a silicone oil model, and reactive Müller glia were isolated by magnetic sorting for transcriptomics. In vitro, Müller glia cultures were treated with a

SUBMITTER: Kumar M 

PROVIDER: S-EPMC12875349 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature