The eye lens consists of epithelial cells, fibre cells and an outer capsule. The\ud epithelium plays a crucial role in maintaining lens growth by continuous cell\ud proliferation and differentiation into fibre cells throughout life. Many studies make or support the assumption that cell organisation within the epithelia of different mammalian lenses follows a common plan, while this has not been studied in detail. To better understand this and how it is associated with the development of posterior capsule opacification (PCO) in the human capsular bag after cataract surgery, I studied some basic cell characteristics in five kinds of mammalian lenses and in human donor capsular bags. The apoptotic cell number was very low in the lens epithelium. Cell density, height, cross-sectional area and volume were different in the three zones of the epithelium, and changed with age in the human lens epithelium. The majority of the cells in the peripheral capsular bag retained their polygonal morphology and were as a single layer. Cell proliferation was mainly restricted to the germinative zone (GZ) in the normal lenses and capsular bags. The proliferation index\ud decreased with age in the human lens epithelium. FGF-2 could initiate cell\ud proliferation by activating the extracellular signal-regulated kinase 1 and 2 (ERK1/2) signalling pathway. An FGF-2 gradient was detected in the inner surface of the bovine lens capsule and its level was statistically higher at the equator where cell proliferation and differentiation occurred. Cell proliferation, cell apoptosis and cell density and size in each zone were all consistent in the young lenses from bovine, mice, rats, rabbits and humans. This suggests that a single model may explain cell organisation in the mammalian lens epithelium and age will be one of its important parameters. Moreover, destroying the residual cell organisation in the peripheral capsular bags might prevent PCO
To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.