# Beta-Catenin in Pseudoexfoliation Syndrome
## 4 Discussion  
To our knowledge, this is the first study assessing the \(\beta\)-catenin concentration in the lens epithelial cells in patients suffering from the cataract and the pseudoexfoliation syndrome, and in patients with the cataract alone. The etiology and pathophysiology of PEX still remain unexplained. For over 17 years, PEX has been considered a systemic disease. For example, PEX was thought to be connected with disorders impairing blood vessels [19]. It is commonly known that vascular calcification is a risk factor for causing cardiovascular events. However, the molecular mechanism underlying this pathogenic process is still obscure. [PERSON] et al. noticed that \(\beta\)-catenin was involved in rat abdominal aortic calcification induced by high Pi. When the knockdown expression of \(\beta\)-catenin in the rat model was investigated, they found that aortic calcification was reduced [8]. Chronic and progressive upregulation of \(\beta\)-catenin is a final pathway common to a wide variety of fibrotic CKDs [20; 21], including diabetic nephropathy, obstructive nephropathy, adriamycin nephropathy, chronic allograft nephropathy, polycystic kidney disease and remnant 5/6-nephrectomy [22]. [PERSON] et al. revealed that protein expression levels of \(\beta\)-catenin were significantly increased by 2.8-fold (\(p=0.002\)) in CKD group kidney tissues compared with the control group [22]. Similarly, our study showed a statistically significant increase in the level of \(\beta\)-catenin in PEX lens epithelial cells (MFI = 808.98) compared to control patients (MFI = 731.6). Furthermore, the analysis of the electronograms from PEX patients showed a larger amount of \(\beta\)-catenin in the cytoplasm of lens epithelial cells. Moreover, in our study, we observed an enhanced accumulation of \(\beta\)-catenin in the area of cell-cell junctions in the PEX group in comparison to the control patients. The increase was confirmed by fluorescence microscope and transmission electron microscope. We suggested that the mechanism of beta-catenin overexpression in PEX cases is associated with the changes in the shape of lens epithelial cells into a flat shape and in the organization of intercellular connections. We observed a change from tight epithelium (TJs) in CTRL to a more point-like pattern of AJs in the PEX patients. As a result, an increase in a level of fluorescence intensity of beta-catenin was noticed. This is a consequence of fact that mentioned types of intercellular junctions are important in contact with neighbouring cells, but they have different structures and functions [23]. Tight junctions are created by occluding and clauds, and are involved in selective barriers and maintaining the polarity of cells [23; 24]. In turn, adherens junctions are formed by the cadherin/catenin complex and play key roles in cell-cell interactions, intracellular signalling and transcriptional regulation [23; 25]. One of the components of AJs, \(\beta\)-catenin, is important in cell adhesion [26]. [PERSON] and [PERSON] also presented the key role of \(\beta\)-catenin in cadherin-based adherens junctions. [27]. Similarly, [PERSON] et al. indicated the involvement of protein in the formation and stabilization of cell-cell junctions [28]. Cited authors described that alterations in beta-catenin caused the destabilization in cell-cell connection [26; 27]. Thus, cell flattening and changes in type of cell-cell junction may induce an increase in the level expression of \(\beta\)-catenin. The presence of point intercellular junctions and a change in epithelial permeability may be associated with an accumulation of pseudoexfoliative material on the anterior lens capsule. In addition, destabilization of cell-cell junctions is common in the cancer metastasis, which is characterized by the loss of contact inhibition, epithelial-to-mesenchymal transition (EMT), and abnormal cell invasiveness [29; 30].