1. Academic Validation
  2. MUC19 expression in human ocular surface and lacrimal gland and its alteration in Sjögren syndrome patients

MUC19 expression in human ocular surface and lacrimal gland and its alteration in Sjögren syndrome patients

  • Exp Eye Res. 2008 Feb;86(2):403-11. doi: 10.1016/j.exer.2007.11.013.
D F Yu 1 Y Chen J M Han H Zhang X P Chen W J Zou L Y Liang C C Xu Z G Liu
Affiliations

Affiliation

  • 1 State Key Laboratory of Ophthalmology of Sun Yat-Sen University, Zhongshan Ophthalmic Center, Ocular Surface Center of Sun Yat-Sen University, Guangzhou, China.
Abstract

This study investigated the expression of MUC19, a newly discovered gel-forming Mucin gene, in normal human lacrimal functional unit components and its alteration in Sjögren syndrome patients. Real-Time PCR and immunohistochemistry were performed to determine the expression of MUC19 and MUC5AC in human cornea, conjunctiva, and lacrimal gland tissues. Conjunctival impression cytology specimens were collected from normal control subjects and Sjögren syndrome patients for Real-Time PCR, PAS staining, and immunohistochemistry assays. In addition, conjunctiva biopsy specimens from both groups were examined for the expression differences of MUC19 and MUC5AC at both mRNA and protein level. The MUC19 mRNA was found to be present in cornea, conjunctiva and lacrimal gland tissues. The immunohistochemical staining of mucins showed that MUC19 was expressed in epithelial cells from corneal, conjunctival, and lacrimal gland tissues. In contrast, MUC5AC mRNA was only present in conjunctiva and lacrimal gland tissues, but not in cornea. Immunostaining demonstrates the co-staining of MUC19 and MUC5AC in conjunctival goblet cells. Consistent with the significant decrease of mucous secretion, both MUC19 and MUC5AC were decreased in conjunctiva of Sjögren syndrome patients compared to normal subjects. Considering the contribution of gel-forming mucins to the homeostasis of the ocular surface, the decreased expression of MUC19 and MUC5AC in Sjögren syndrome patients suggested that these mucins may be involved in the disruption of the ocular surface homeostasis in this disease.

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