TISSUE TRANSGLUTAMINASE IN APOPTOSIS OF PHOTORECEPTOR CELLS IN RAT RETINA

Citation
Sr. Zhang et al., TISSUE TRANSGLUTAMINASE IN APOPTOSIS OF PHOTORECEPTOR CELLS IN RAT RETINA, Investigative ophthalmology & visual science, 37(9), 1996, pp. 1793-1799
Citations number
25
Categorie Soggetti
Ophthalmology
ISSN journal
01460404
Volume
37
Issue
9
Year of publication
1996
Pages
1793 - 1799
Database
ISI
SICI code
0146-0404(1996)37:9<1793:TTIAOP>2.0.ZU;2-S
Abstract
Purpose, The possible involvement of tissue transglutaminase (tTG) in apoptosis during photoreceptor degeneration was examined in retinal ph otic injury in rats and in retinal dystrophy of Royal College of Surge ons (RCS) rats. Methods, Retinal photic injury was induced in 48 male Lewis albino rats by exposure to green fluorescent light of 300 to 320 foot-candles. The retinal tTG was examined by enzyme assay, immunohis tochemistry, and Western blot analysis after 9, 12, or 24 hours of exp osure or at 6 or 24 hours of dark adaptation after 24 hours of light e xposure. Retinas from RCS rats at various stages of degeneration also were examined with similar methods. Results, There was a progressive i ncrease in retinal tTG activity after 300 to 320 ft-c of light exposur e, reaching a peak after 24 hours of light exposure. In the RCS rats, tTG activity increased with age. Western blot analysis revealed an imm unoreactive band at 80 kDa, which increased in accordance with the tra nsglutaminase activity in both models. In normal, rat retinas, tTG imm unolabeling was present only in the outer segments. There was an incre ased number of immunolabeled photoreceptor nuclei from 12 hours of lig ht exposure to 24 hours of light exposure. In the RCS rat, increasing numbers of immunopositive photoreceptor nuclei from 20 to 50 days of a ge were noted. Conclusions. The data associated increased retinal tTG activity and enzyme levels with photoreceptor cells undergoing apoptos is. The tTG-dependent irreversible cross-linking of intracellular prot ein may play an important role in causing the structural changes in ce lls undergoing apoptosis in the retina.