Meibomian gland dysfunction. II. The role of keratinization in a rabbit model of MGD.
Meibomian gland dysfunction. II. The role of keratinization in a rabbit model of MGD.
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发表时间：
1989-05
影响因子：
4.4
通讯作者：
J. Jester;N. Nicolaides;I. Kiss-Palvolgyi;R. E. Smith
中科院分区：
文献类型：
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作者：
J. Jester;N. Nicolaides;I. Kiss-Palvolgyi;R. E. Smith
34只白化病家兔用2%肾上腺素每日2次局部注射，连续6个月至1年，造成睑板腺功能障碍（MGD）。7只年龄匹配的对照兔（未接受肾上腺素）随访相似时间。通过大体临床检查和透照生物显微镜和摄影对治疗前后的所有眼睑进行评价。在评价的68只兔眼睑中，56%出现MGD体征，范围从睑板腺口堵塞和存在微囊肿（亚临床病变; 30.9%的眼睑）到腺体混浊和增大，严重程度增加（临床病变; 25.0%的眼睑）。其余眼睑（44%）保持正常。在7只对照兔中未发生MGD。在MGD发展后，通过免疫荧光显微镜、SDS-PAGE和使用小鼠角蛋白单克隆抗体的Western印迹来评价眼睑。兔MGD的发生和进展似乎与睑板腺导管上皮的分层和角化增加相关。在MGD的早期阶段，上皮过度角化的焦点区域通过使用AE 2单克隆抗体的免疫组织化学染色来鉴定，AE 2单克隆抗体特异于角化表皮的56.5kD和65-67 kD角蛋白蛋白标记物。随着MGD严重程度的进展，导管上皮的AE 2染色逐渐增加。慢性MGD患者睑板腺排泄物蛋白的SDS-PAGE和免疫印迹显示，在MGD发展过程中，56.5 kD和65-67 kD角化蛋白标记物均逐渐增加。我们的结论是，过度角化的导管上皮细胞导致堵塞和扩张的睑板腺的基础发展MGD后局部肾上腺素治疗。
Meibomian gland dysfunction (MGD) was induced in 34 albino rabbits by the twice-daily topical application of 2% epinephrine over a period of 6 months to 1 year. Seven age-matched control rabbits, not receiving epinephrine, were followed up for a similar period. All lids were evaluated pre- and post-treatment by gross clinical examination and by transillumination biomicroscopy and photography. Of the 68 rabbit lids evaluated, 56% developed signs of MGD, which ranged from plugging of the meibomian gland orifice and presence of microcysts (subclinical lesions; 30.9% of the lids) to opacification and enlargement of the glands with increasing severity (clinical lesions; 25.0% of the lids). The remaining lids (44%) remained normal. MGD did not develop in the seven control rabbits. After the development of MGD, lids were evaluated by immunofluorescent microscopy, SDS-PAGE and Western blotting using mouse monoclonal antibodies to keratin proteins. Development and progression of MGD in the rabbit appears to correlate with increasing stratification and keratinization of the meibomian gland duct epithelium. In the early stages of MGD, focal areas of epithelial hyperkeratinization were identified by immunohistochemical staining using AE2 monoclonal antibody, specific for the 56.5 kD and 65-67 kD keratin protein marker for keratinized epidermis. As the severity of MGD progressed there was progressive increase in the AE2 staining of the duct epithelium. SDS-PAGE and immunoblotting of proteins from meibomian gland excreta in chronic MGD showed a progressive increase in both the 56.5 kD and 65-67 kD keratinization protein markers during development of MGD. We conclude that hyperkeratinization of the duct epithelium leading to plugging and dilation of the meibomian gland underlies the development of MGD following topical epinephrine treatment.