May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Role of MAP3K1 in Mouse Postnatal Eye Development
Author Affiliations & Notes
  • W. W. Y. Kao
    University of Cincinnati, Cincinnati, Ohio
    Ophthalmology,
  • M. Mongan
    University of Cincinnati, Cincinnati, Ohio
    Environmental Health,
  • H. Liu
    University of Cincinnati, Cincinnati, Ohio
    Ophthalmology,
  • Y. Xia
    University of Cincinnati, Cincinnati, Ohio
    Environmental Health,
  • Footnotes
    Commercial Relationships  W.W.Y. Kao, None; M. Mongan, None; H. Liu, None; Y. Xia, None.
  • Footnotes
    Support  Grants from NIH EY015227, EY013755, Research to Prevent Blindness, Ohio Lions Eye Research Foundation
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 3461. doi:https://doi.org/
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    • Get Citation

      W. W. Y. Kao, M. Mongan, H. Liu, Y. Xia; Role of MAP3K1 in Mouse Postnatal Eye Development. Invest. Ophthalmol. Vis. Sci. 2008;49(13):3461. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : Mitogen-activated protein kinase kinase kinase 1 (MAP3K1) is involved in signal transduction in tissue morphogenesis during development. MAP3K1 ablation in mice results in defective eyelid development with characteristic eye open at birth (EOB) phenotype. Since the EOB inflicts secondary ocular tissue damages after birth, e.g., exposure keratitis, it remains unclear whether MAP3K1 ablation affects other ocular tissue development at postnatal stages.

Methods: : To mimic the postnatal eyelid status of the wild type mice, we sutured the eyelid Map3k1 ΔKD/ ΔKD mice eyelids immediately after birth and removed the suture at postnatal day 15. Conversely, we surgically opened the closed eyelids of wild type mice at birth to mimic the eyelid status of the Map3k1 ΔKD/ ΔKD mice. At postnatal day 15, eyes were isolated and processed for paraffin embedding. H&E staining and immunohistochemistry were performed on 4 um sections of the eyes to characterize the development of ocular tissues, including cornea, lens, meibomian glands and retina.

Results: : In both wild type and Map3k1 ΔKD/ ΔKD mice, an opened eye from P1-15 was associated with ocular surface pathologies, including thickening and vascularization of the corneal stroma with infiltration of inflammatory cells and disruption of stromal collagen fiber organization, lacking keratin 12 expression in corneal epithelial cells, and loss of the anterior chamber angle. There was also an adverse consequence of the opened eyelid on meibomian gland and lens development. The eyelid suture of the Map3k1ΔKD/ ΔKD mice had significantly improved clinical manifestations, e.g., keratitis, but did not completely restore normal ocular morphology. The Map3k1ΔKD/ ΔKD mice with and without eyelid suturing showed retinal abnormalities, including areas of folding between the rods and cones and the outer nuclear layers and increased cell numbers in the inner plexiform layer. Interestingly, the retina abnormalities were specific to the Map3k1ΔKD/ ΔKD, not seen in the wild type mice even if their eyelids were surgically opened at birth and developed ocular surface pathologies.

Conclusions: : MAP3K1 plays a role in the postnatal retina development.

Keywords: eyelid • development • signal transduction 
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