Repair and reconstruction of the mouse lens after perforating injury.
OBJECTIVE
To investigate the process of repair in the epithelial cells and the reconstruction in lens fibers of a mouse lens that has developed opacity because of a large-scale perforating injury.


METHODS
Lenses of 4-week-old mice were perforated with a needle through the cornea to induce the development of traumatic cataracts. Over the period from the first day to the fifth month after injury, eyeballs were extracted progressively from the mice and changes in the epithelial cells of these lenses were observed morphologically as well as histochemically.


RESULTS
Following the injury, the epithelial cells of the lenses extended toward the center of the injury, while undergoing repeated proliferation and stratification. After a month, the epithelial cells completely covered the entire injury. Later, a basal lamina and collagen fibers developed among the epithelial cells that had proliferated, the intracellular space enlarged, but the number of cells decreased. Histochemically, a strong actin-positive finding was observed in the epithelial cells in the growth phase. On the other hand, an investigation by means of the TUNEL method revealed epithelial cell death and a decrease in cell number. Maximal cell death was observed in the second month. During this period, lens fibers regenerated, and the clear areas of the cortex increased.


CONCLUSIONS
Although the lenses exhibited opacity over a large area, the epithelial cells eventually fully covered the injured area. Once the repair was completed, the number of epithelial cells decreased. At the same time, the lenses were found to have developed increased clarity, leading to reconstruction. The epithelial recovery and the residual posterior suture may be the key to the reconstruction of the lenses.
Hirayama
Sawori
S
Departments of Ophthalmology, Graduate School of Medical Sciences, Kitasato University, Kanagawa, Japan. sawori@f2.dion.ne.jp
Wakasugi
Akino
A
Morita
Tetsuya
T
Sakai
Yasuhiro
Y
Mukuno
Kazuo
K
Uga
Shigekazu
S
Shimizu
Kimiya
K
D000199:Actins / Q000378:metabolism; D000818:Animals; D001485:Basement Membrane / Q000648:ultrastructure; D002386:Cataract / Q000473:pathology*; D002452:Cell Count; D016923:Cell Death; D003094:Collagen / Q000648:ultrastructure; D004247:DNA / Q000096:biosynthesis; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000378:metabolism / Q000648:ultrastructure*; D015807:Eye Injuries, Penetrating / Q000473:pathology*; D005260:Female; D020287:In Situ Nick-End Labeling; D007908:Lens, Crystalline / Q000293:injuries* / Q000378:metabolism / Q000648:ultrastructure*; D051379:Mice; D014945:Wound Healing
D000199:Actins; D003094:Collagen; D004247:DNA