RESUMO
Cataract is lens opacity, which is a common blinding eye disease worldwide. Aquaporin 5 (AQP5) is expressed in the human and mouse lenses. This study aimed to investigate the underlying mechanisms of AQP5 in the senescence of lens epithelial cells (LECs). Primary LECs were isolated and cultured from Aqp5+/+ and Aqp5-/- mice. Western blot or immunofluorescence staining of p16, Ki67, MitoSOX, JC-1 and phalloidin was used in the experiments to evaluate the changes in the primary LECs. The primary Aqp5-/- LECs showed increased p16 expression and mitochondrial reactive oxygen species, decreased mitochondrial membrane potential and activity, and cytoskeletal disorders. When the cells were pretreated with Mito-TEMPO, the Aqp5-/- mice showed decreased p16 expression, reduced mitochondrial dysfunction and cytoskeletal disorders. Our results revealed that AQP5 deficiency promotes the senescence of primary LECs through mitochondrial dysfunction. This provides a new perspective for the treatment of cataracts by regulating AQP5 expression.
RESUMO
As a water channel protein, aquaporin 5 (AQP5) is essential for the maintenance of the normal physiological functions of ocular tissues. This review provides an overview of the expression and function of AQP5 in the eye and discusses their role in related eye diseases. Although AQP5 plays a vital role in ocular functions, such as maintaining corneal and lens transparency, regulating water movement, and maintaining homeostasis, some of its functions in ocular tissues are still unclear. Based on the key role of AQP5 in eye function, this review suggests that in the future, eye diseases may be treated by regulating the expression of aquaporin.