May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
Misexpression of Proneural Gene Ash1 Alters the Structure of Corneal Stroma in the Chick Eye
Author Affiliations & Notes
  • W. Mao
    University of Alabama at Birmingham, Birmingham, AL
    Vision Science Graduate Program,
  • S.–Z. Wang
    University of Alabama at Birmingham, Birmingham, AL
    Department of Ophthalmology,
  • Footnotes
    Commercial Relationships  W. Mao, None; S. Wang, None.
  • Footnotes
    Support  NIH EY11640, RPB, and EyeSight Foundation of Alabama
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 3008. doi:
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      W. Mao, S.–Z. Wang; Misexpression of Proneural Gene Ash1 Alters the Structure of Corneal Stroma in the Chick Eye . Invest. Ophthalmol. Vis. Sci. 2006;47(13):3008.

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Abstract

Purpose: : To study the role of proneural bHLH gene ash1 in embryonic chick corneal development.

Methods: : Replication–competent retrovirus RCAS was used to drive chick ash1 or GFP misexpression in the developing chick eye. Embryonic corneas were fixed, sectioned, and analyzed with hematoxylin–eosin staining and immunocytochemical staining.

Results: : RCAS–driven misexpression of ash1 in the chick cornea resulted in corneal extrusion. The integrity of corneal epithelial layer and endothelial layer was not disturbed. However, the thickness of corneal stroma increased significantly, and this thickening was maintained in older embryos. We found extensive swelling of both anterior acellular and posterior cellular regions, and the swelling might have contributed to the corneal stroma thickening. In the cellular region, cells were disorganized and sparsely distributed, while the overall number of cells showed no significant increase. The corneal fibroblasts were morphologically abnormal, and their cytoplasmic processes were much extended.

Conclusions: : Our gain–of–function experiments showed perturbation in corneal development from ash1 misexpression. The extruded, thickened cornea might have resulted from a failure in cornea compaction, possibly due to abnormal expression of extracellular matrix molecules. Our results suggest that ash1 may play a role in regulating corneal development. Such a hypothesis is consistent with ash1’s known function in regulating the genesis of neural crest–derived, PNS neurons, since corneal formation also involves the participation of neural crest–derived cells.

Keywords: development • cornea: stroma and keratocytes • transcription factors 
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