Immunohistochemical Profiles of LOXL-1, FBN1, TGF-β1, and COX-2 in Pseudoexfoliation Syndrome

ABSTRACT

Purposes: To (i) determine expression patterns of lysyl oxidase-like 1 (LOXL1), fibrillin-1 (FBN1), transforming growth factor beta-1 (TGF-β1), and cyclooxygenase-2 (COX-2) in lens epithelium and anterior lens capsule in pseudoexfoliation (PEX) syndrome and (ii) delineate the roles of these proteins in the etiopathogenesis of PEX.

Materials and methods: Study participants, all of whom had undergone cataract surgery, comprised 47 patients with and 27 patients without (controls) PEX syndrome. Immunohistochemistry on paraffin sections of lens capsule and lens epithelium was performed.

Results: Immunoexpression of LOXL1 and FBN1 on the outer surface of the lens capsule was significantly higher (p < 0.001), and nuclear immunopositivity for LOXL1 was more frequently observed (p = 0.017), in PEX patients compared with control patients. Cytoplasmic expression of LOXL1 and COX-2 was significantly lower (p = 0.015 and p = 0.042, respectively) in PEX patients compared with controls. TGF-β1 exhibited diffuse immunostaining detected in all cell layers in PEX patients (p <0.001). Significant direct correlations of cytoplasmic LOXL1 with FBN1 and TGF-β1, and of COX-2 with FBN1, TGF-β1, and LOXL-1, were observed only in PEX patients.

Conclusions: Results of our study provide valuable information vis-à-vis expression and localization of TGF-β1, LOXL1, and FBN1, as well as their associations in the lens epithelium and lens capsule. These data not only advance our knowledge of the etiopathogenesis of PEX syndrome, but also include novel findings, for example, immunostaining patterns of TGF-β1 in PEX syndrome. We suggest that COX-2 plays a role in the pathobiology of PEX syndrome and should be the subject of future investigations.

KEYWORDS:

• LOXL1
• FBN1
• COX-2
• TGF-β1
• immunohistochemistry
• pseudoexfoliation syndrome

Declaration of interest

The authors report no conflict of interests and are responsible for the content and writing of the paper.