Cell Biological Analysis with Respect to Cause of Fibrous Opacification of the Anterior Capsule after Cataract Extraction

Abstract

It has been assumed that lens epithelial cells (LECs) existing at the capsulotomy edge have been traumatized through anterior capsulotomy in cataract extraction. In this study, the correlation between traumatized LECs remaining at the anterior capsulotomy edge and epidermal growth factor (EGF) found in the aqueous humor, a cell growth factor though to affect cell morphology, was determined. Anterior lens capsules with adhering LECs were obtained following anterior capsulotomy performed during cataract surgery to first confirm the presence of EGF receptors on LECs, which are needed for EGF to be biologically active. Besides, to identify any EGF receptors on traumatized LECs, I next intentionally traumatized the cells by pressing them with a forceps from the anterior capsular side. It has been found that the LECs containing EGF receptors were always those existing at the edge of the anterior capsular opening and LECs containing EGF receptors existed along the pressed region too. The present results indicate that traumatized LECs along the capsulotomy edge have undergone changes to manifest EGF receptors, thus allowing EGF from the aqueous humor to become more active. The physiological effect of EGF upon these LECs may therefore be one of the causative factors of fibrous opacification of the anterior capsulotomy edge after cataract extraction.

EGFR-Blockade With Erlotinib Reduces EGF and TGF-β2 Expression and the Actin-Cytoskeleton Which Influences Different Aspects of Cellular Migration in Lens Epithelial cells

“…6,7 EGF/EGFR signaling is associated with PCO. [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22] EGFR is expressed in the natural human lens epithelium 17 constantly throughout different age groups. 15 Previously, we have demonstrated that the selective EGFR inhibitor Erlotinib (Tarceva Õ , OSI-774, Roche; tyrosine kinase inhibitor; HER1-and Erb-1-receptor inhibitor) 23 mitigates HLEC proliferation, migration, collagen matrix contraction and cell spreading in vitro, which represent the crucial cellular events of PCO formation.…”