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Essential role for c-Jun N-terminal kinase 2 in corneal epithelial response to desiccating stress

Cintia S De Paiva1, Solherny B Pangelinan, Emmanuel Chang

  • 1Ocular Surface Center, Cullen Eye Institute, Baylor College of Medicine, 6565 Fannin St, NC 205, Houston, TX 77030, USA. cintiadp@bcm.tmc.edu

Archives of Ophthalmology (Chicago, Ill. : 1960)
|December 17, 2009
PubMed
Abstract

Insights

Gene knockout of JNK2 protects the cornea from dry eye disease. JNK2 knockout mice showed reduced corneal damage and inflammation, suggesting JNK2 as a therapeutic target for dry eye.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Cell Biology

Background:

  • Desiccating stress (DS) can cause corneal epithelial damage.
  • c-Jun N-terminal kinase (JNK) signaling pathways are involved in cellular responses to stress.

Purpose of the Study:

  • To investigate the protective effects of JNK-1 and JNK-2 gene knockout (KO) on the corneal epithelium under desiccating stress.
  • To elucidate the role of JNK2 in the pathogenesis of desiccation-induced corneal epithelial disease.

Main Methods:

  • Mice lacking JNK1 or JNK2 (JNK1KO, JNK2KO) and wild-type (C57BL/6) controls were exposed to desiccating stress for 5 days.
  • Corneal smoothness, permeability, matrix metalloproteinases (MMP)-1, MMP-9, cornified envelope protein precursors (SPRR-1a, SPRR-2a, involucrin) expression, and enzyme activity were assessed.

Main Results:

  • JNK2KO mice exhibited smoother corneas and less barrier disruption compared to JNK1KO and wild-type mice after DS.
  • DS increased MMPs and cornified envelope precursors in JNK1KO and wild-type mice, but not in JNK2KO mice.
  • JNK2 knockout prevented DS-induced increases in corneal gelatinase and collagenase activity.

Conclusions:

  • JNK2 plays a critical role in desiccation-induced corneal epithelial disease by promoting MMP and cornified envelope precursor production.
  • JNK2 inhibition represents a potential therapeutic strategy for managing dry eye disease.

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