Abstract
Purpose :
Ultraviolet B (UVB) is a significant risk factor to cause lens epithelium damage; however, the mechanism of lens epithelium repair after UVB irradiation is not fully understood. This study aimed to investigate the mechanism of the lens epithelium-mediated repair process after UVB irradiation.
Methods :
C57BL/6J mice were irradiated by various doses of UVB. Lens cataracts were examined at different time points by slit lamp, darkfield microscopy, and phase-contrast microscopy. Lens epithelial cell (LEC) mitotic activation and apoptosis was determined by immunofluorescence staining and LECs’ ultrastructure was analyzed by TEM.
Results :
UVB irradiation above a dose of 2.87 kJ/m2 triggered LECs apoptosis and subcapsular cataract formation associated with a ring-shaped structure composed of multilayered and irregularly stacked epithelial cells. LECs around wound edges transitioned to mitotically active cells reflected by increased Ki67 expression and BrdU incorporation. These mitotic active LECs performed wound-healing repair through the epithelialization process and removed apoptotic cells via phagocytosis. However, repairs ceased when lens epithelial cells made direct contact, and scar-like tissue in the center of the anterior capsule remained even by six months after UVB irradiation.
Conclusions :
Our present study demonstrates that normally quiescent lens epithelial cells can be reactivated for epithelialization repair in response to UV-induced damage.
This abstract was presented at the 2022 ARVO Annual Meeting, held in Denver, CO, May 1-4, 2022, and virtually.