Abstract
Purpose:
A membrane-bound mucin, Muc16, is expressed in conjunctiva in mice. We examined the effects of the loss of conjunctival Muc16 in the structure and behavior of corneal epithelium in mice.
Methods:
(1) Histology at light and electron microscopic levels and immunohistochemistry of the corneal epithelium of 26 wild-type (WT) and 16 Muc16-null (KO) mice was performed. Shape of the nuclei in basal and suprabasal later was observed to know the differentiation of suprabasal cells. TUNEL stain and BrdU-evaluation of cell proliferation were also included. (2) Healing of a round defect in corneal epithelum was evaluated in WT (n = 24) and KO (n = 24) mice at intervals of healing up to 30 hrs.
Results:
1) Light and electron microscopies showed an impairment of differentiation of suprabasal cells. The nuclei of the suprabasal cells exhibited a more round shape in a KO mouse as compared with them in a WT epithelium. Keratin 14 was detected in both basal and suprabasal cells in a KO epithelium, while restricted to the basal cells in a WT mouse. Cell proliferation was more marked in a KO mouse than in 1 WT mouse. TUNEL-labeled cells were not obsderved in both WT and KO mice. (2) healing of a round defect in corneal epithelium was significantly promoted by lacking Muc16.
Conclusions:
Cell proliferation enhancement and the presence of keratin 14-positive cells with a relatively round nuclei in the suprabasal layer suggests the acceleration of intraepithelial cell turnover in mice lacking Muc16 in conjunctiva. The loss of Muc16 indirectly affected wound healing (migration) in corneal epithelium in mice.
Keywords: 482 cornea: epithelium •
765 wound healing •
500 differentiation