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Related Experiment Video

Updated: Mar 28, 2026

A Magnetic Microbead Occlusion Model to Induce Ocular Hypertension-Dependent Glaucoma in Mice
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Macrophage Migration Inhibitory Factor (MIF)-CD74 Signaling Pathway Mediates Trabecular Meshwork Dysfunction in

Monu Monu1, Lal Krishan Kumar1, Prince Kumar1

  • 1Department of Ophthalmology, Mason Eye Institute, University of Missouri School of Medicine, Columbia, Missouri, USA.

Biorxiv : the Preprint Server for Biology
|March 27, 2026
PubMed
Summary
This summary is machine-generated.

Macrophage migration inhibitory factor (MIF) signaling drives trabecular meshwork dysfunction in primary open-angle glaucoma by suppressing Blimp-1. Inhibiting MIF restores TM function and may offer new glaucoma treatments.

Keywords:
4-IPPBlimp-1CD74GlaucomaMIFTGF-β2agmatinefibroticintraocular pressuremyocilinthiaminetrabecular meshwork

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Area of Science:

  • Ophthalmology
  • Immunology
  • Cell Biology

Background:

  • Macrophage migration inhibitory factor (MIF) is a cytokine involved in inflammatory and fibrotic diseases.
  • The role of MIF in primary open-angle glaucoma (POAG) and trabecular meshwork (TM) dysfunction is currently unknown.
  • Understanding MIF's role in TM pathology is crucial for developing new glaucoma therapies.

Purpose of the Study:

  • To investigate the role of MIF-CD74 signaling in TM pathobiology.
  • To determine if MIF-CD74 signaling modulates the transcription factor Blimp-1.
  • To examine the downstream effects on cytoskeletal reorganization and extracellular matrix (ECM) remodeling in TM cells.

Main Methods:

  • Primary human TM cells (HTMC) were treated with glaucomatous stressors (TGF-β2, rMIF, pro-inflammatory milieu).
  • MIF, CD74, and Blimp-1 expression were quantified using qPCR and immunoblotting.
  • ECM proteins, pMLC, and MIF-CD74/Blimp-1 expression were assessed in mouse models of ocular hypertension (OHT).
  • Functional effects were evaluated using MIF inhibitors and immunomodulatory metabolites.

Main Results:

  • Glaucomatous stressors increased MIF and CD74 expression while decreasing Blimp-1 in HTMC and OHT mouse models.
  • MIF-CD74 activation promoted inflammation, cell death, and ECM remodeling, including increased fibrotic proteins and RhoA/ROCK-mediated pMLC.
  • MIF inhibition reduced inflammatory signaling, ECM deposition, and cytoskeletal remodeling, restoring a protective TM phenotype.

Conclusions:

  • MIF-CD74 signaling is a novel regulator of TM dysfunction in POAG.
  • MIF suppresses Blimp-1, linking inflammation to TM contractility and ECM remodeling, thereby increasing outflow resistance.
  • Targeting the MIF-CD74/Blimp-1 axis presents a potential therapeutic strategy for glaucoma to restore TM homeostasis and reduce intraocular pressure.