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Macrophages Transdifferentiate Into Myofibroblasts During Ocular Surface Inflammation.

Nishant R Sinha1, Vinay K Pulimamidi1, Olufemi S Folorunso1

  • 1Department of Ophthalmology, Harvard Medical School, Schepens Eye Research Institute of Massachusetts Eye and Ear, Boston, Massachusetts, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|May 23, 2025
PubMed
Summary
This summary is machine-generated.

Macrophages can transform into myofibroblast-like cells during ocular surface inflammation and injury. These alpha-smooth muscle actin (ɑ-SMA)+ macrophages contribute to fibrosis by remodeling extracellular matrix (ECM), impacting vision.

Keywords:
corneafibrosismacrophagemyofibroblastsocular surface

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Area of Science:

  • Ophthalmology
  • Immunology
  • Cell Biology

Background:

  • Ocular surface inflammation and injury can cause fibrosis and vision loss.
  • Myofibroblasts drive fibrosis by producing extracellular matrix (ECM) and alpha-smooth muscle actin (ɑ-SMA).
  • Macrophages are known to promote fibrosis, but their direct ECM remodeling capacity is unclear.

Purpose of the Study:

  • To investigate if macrophages transdifferentiate into myofibroblast-like cells during ocular surface inflammation.
  • To analyze the role of macrophages in corneal fibrosis and ECM remodeling.

Main Methods:

  • Utilized a mouse model of corneal injury and fibrosis.
  • Quantified F4/80+ɑ-SMA+ macrophages during wound healing and remodeling stages.
  • Activated human and mouse macrophages in vitro with pro-fibrotic cytokines (IL-10, TGF-β1).
  • Assessed macrophage phenotype, ECM/cytoskeletal protein expression, and collagen gel contraction.

Main Results:

  • F4/80+ɑ-SMA+ macrophages increased during corneal wound healing and remodeling.
  • Macrophage transition correlated with the shift from inflammatory to pro-fibrotic microenvironment.
  • In vitro, activated macrophages adopted myofibroblast characteristics (spindle shape, ɑ-SMA, desmin, fibronectin, collagen III expression).
  • ɑ-SMA+ macrophages demonstrated significant collagen gel contraction, functionally mimicking myofibroblasts.

Conclusions:

  • Macrophages possess the capacity to transdifferentiate into myofibroblasts in the context of ocular surface inflammation.
  • This macrophage transdifferentiation contributes to fibrosis and ECM remodeling in ocular injuries.
  • Findings suggest a novel cellular mechanism in ocular surface fibrosis progression.