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Shin Mizoguchi, Yuka Okada, Reiko Arita, Geraint John Parfitt, Yilu Xie, James V Jester, Shizuya Saika; Ductal dilation with Meibum retention and decreased expression of PPARγ in Meibomian gland following ocular surface alkali injury in mice. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2507.
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© ARVO (1962-2015); The Authors (2016-present)
We previously reported Meibomian gland duct is dilated following ocular surface alkali injury and that this finding is independent of Smad3 signaling in mice. The purpose of this study was to examine the morphological changes within the Meibomian gland by using 3D image and expression pattern of PPARγ.
Ocular surface alkali burn was produced by topical application of 1N NaOH in one eye of adult C57BL/6 mice. Following healing intervals of 5, 10 and 20 days, 5, the animals were killed and the upper and lower eyelids were excised. Meibomian glands were observed in both upper and lower eyelids under binocular microscope. Meibomian glands were embedded in BMMA plastic and serially section of immunofluorescent tomography (IT) and 3 dimensional reconstruction using software Amira®. Another sets of specimens were processed for cryosectioning and oilred O staining or for paraffin sections for ommunoshitochemistry for PPARγ.
As early as day 5 post-alkali burn, marked dilation of Meibomian gland duct was observed in 3D reconstructions. Oil red O staining showed the substance in the dilated duct to contain neutral lipid, presumably Meibum. Dilation was also associated with a marked reduction in PPARγ of meibocytes of alkali-burned mice as compared to uninjured normal Meibomian glands.
Ocular surface alkali injury leads to Meibomian gland ductal dilation and down regulation of PPARγ suggesting loss of meibocyte differentiation. These findings suggest that alkali injury leads to obstruction of the meibomian gland orifice and down stream dilation and atrophy of meibocytes.
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