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Lipoxin B4 Mitigates TRPV4-Activated Müller Cell Gliosis During Ocular Hypertension

Matangi Kumar1,2, Shruthi Karnam2, Shubham Maurya2

  • 1Vision Science Graduate Group, University of California Berkeley, Berkeley, California, United States.

Investigative Ophthalmology & Visual Science
|February 2, 2026
PubMed
Abstract

Insights

Müller glia produce lipoxin B4 (LXB4), a neuroprotective mediator that suppresses glial reactivity. This study shows LXB4 counter-regulates TRPV4-induced Müller glia activation, offering a potential glaucoma treatment target.

Area of Science:

  • Neuroscience
  • Ophthalmology
  • Cell Biology

Background:

  • Müller glia are crucial for retinal homeostasis but contribute to neuroinflammation in glaucoma.
  • Elevated intraocular pressure activates Müller glia via TRPV4 channels, leading to retinal ganglion cell loss.
  • Lipoxin B4 (LXB4), produced by astrocytes, can suppress glial reactivity and protect retinal ganglion cells.

Purpose of the Study:

  • To investigate if LXB4 modulates TRPV4-mediated Müller glia activation.
  • To determine if Müller glia contribute to the lipoxin pathway.

Main Methods:

  • Induction of ocular hypertension in mice.
  • Isolation of reactive Müller glia for transcriptomic analysis.
  • In vitro treatment of Müller glia cultures with TRPV4 agonist and LXB4.
  • Assessment of glial reactivity using flow cytometry, immunostaining, qPCR, and Western blotting.
  • Lipidomics and single-cell RNA sequencing to analyze pathway metabolites and transcriptional responses.

Main Results:

  • Müller glia express 5- and 15-lipoxygenase, producing endogenous LXB4.
  • TRPV4 activation induced gliosis, increasing GFAP, IL-6, and STAT3 expression, and lipoxin production.
  • LXB4 suppressed TRPV4-induced gliosis in vitro and in vivo by downregulating inflammatory markers and attenuating TRPV4 upregulation.

Conclusions:

  • Müller glia are a significant source of the neuroprotective mediator LXB4.
  • The LXB4 pathway in Müller glia is amplified during TRPV4 activation to counteract gliosis.
  • Targeting the TRPV4-lipoxin pathway presents a potential therapeutic strategy for glaucoma.

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