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Release of membrane-associated mucins from ocular surface epithelia

Timothy D Blalock1, Sandra J Spurr-Michaud, Ann S Tisdale

  • 1Schepens Eye Research Institute and Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA.

Investigative Ophthalmology & Visual Science
|April 26, 2008
PubMed
Abstract

Insights

Tear components like neutrophil elastase and TNF can release membrane-associated mucins (MAMs) from the ocular surface. This release may impact the eye

Area of Science:

  • Ocular surface biology
  • Epithelial cell research
  • Tear film proteomics

Background:

  • Three membrane-associated mucins (MAMs)—MUC1, MUC4, and MUC16—are crucial for ocular surface health.
  • Soluble MAMs are found in tears, but their release mechanisms are unclear.

Purpose of the Study:

  • To identify physiological agents that trigger the release of ocular surface MAMs.
  • Investigate the role of specific tear components in mucin shedding.

Main Methods:

  • Utilized an immortalized human corneal-limbal epithelial cell line (HCLE).
  • Assessed the effects of neutrophil elastase, tumor necrosis factor (TNF), and matrix metalloproteinases (MMPs) on HCLE cells.
  • Measured MAM release, surface restoration, and barrier function using biotinylation and rose bengal dye exclusion.

Main Results:

  • TNF induced the release of MUC1, MUC4, and MUC16.
  • Neutrophil elastase and MMP-7 released MUC16, but not MUC1 or MUC4.
  • Neutrophil elastase treatment led to significant MUC16 shedding and reduced ocular surface barrier function.

Conclusions:

  • Extracellular domains of MUC1, MUC4, and MUC16 can be released from the ocular surface by tear components.
  • Elevated levels of neutrophil elastase and TNF in dry eye tears may contribute to MAM release and compromised barrier function.

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