Melatonin Type 2 Receptor Activation Regulates Blue Light Exposure-Induced Mouse Corneal Epithelial Damage by

Rujun Jin1, Ying Li1, Hui Jin1,2

  • 1Department of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju 61469, Korea.

Insights

Blue light (BL) exposure increases MT2 receptor expression in mouse corneas, impacting autophagy and apoptosis. MT2 receptor activation worsens blue light-induced corneal epithelial damage.

Area of Science:

  • Ophthalmology
  • Neuroscience
  • Cell Biology

Background:

  • Melatonin receptors (MT1/2) are G protein-coupled receptors regulating circadian rhythms.
  • MT1/2 receptors are implicated in mitochondrial homeostasis, antioxidant, and anti-inflammatory responses in various tissues.
  • The role of MT1/2 receptors in corneal health and response to environmental stressors like blue light is not well understood.

Purpose of the Study:

  • To investigate the effects of blue light (BL) exposure on melatonin and MT1/2 receptor expression in the mouse cornea.
  • To evaluate the functional role of MT1/2 receptors in blue light-induced corneal epithelial damage.

Main Methods:

  • 8-week-old C57BL/6 mice were exposed to blue light (25 and 100 J/cm² twice daily for 14 days).
  • Expression levels of 4-hydroxynonenal (4-HNE), MT2, p62, BAX, and cleaved caspase 3 were analyzed.
  • Mice were treated with an MT2 antagonist to assess its protective effects against blue light damage.
  • Malondialdehyde (MDA) levels and corneal damage were evaluated.

Main Results:

  • Blue light exposure significantly increased 4-HNE and MT2 expression in the cornea.
  • MT2 antagonist treatment in BL-exposed mice led to increased p62 and decreased BAX and cleaved caspase 3 expression.
  • MT2 antagonist treatment ameliorated MDA levels and reduced corneal damage compared to BL-exposed mice without antagonist.

Conclusions:

  • Blue light exposure induces MT2 receptor expression in the mouse cornea.
  • MT2 receptor activation modulates impaired autophagy and apoptosis by upregulating BAX, thus promoting corneal epithelial damage.
  • Targeting MT2 receptors may offer a therapeutic strategy for blue light-induced ocular surface damage.

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