Corneal endothelial cells are derived from the neural crest and form the corneal endothelial lining as a single layer of hexagonal cells that are believed not to proliferate throughout a person's lifetime.1'2 Thus, wound healing in the human corneal endothelium is accomplished mainly by cell spreading, and the number of human corneal endothelial cells (HCECs) decreases with a person's age.1'2 Mimura and Joyce3 demonstrated that HCECs in younger donors have little senescence-associated beta-galactosidase (SA-(3-gal) activity in either the central or peripheral areas. On the other hand, SA-beta-gal activity is easily detectable in corneas from older donors, in whom the central HCECs show stronger S A-beta-gal activity than the peripheral HCECs.3 These results suggest that HCECs age with senescence. Are the senescence-related mechanisms of HCECs in vivo associated with the shortening of the telomeres or with the accumulation of cellular damage?
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