December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Cell proliferation and Apoptosis in Vitreoretinal Disorders( PVR, PDR, Macular Pucker): Expression of Ki-67( MIB-1), PCNA, Cyclin E, CDK4, Caspase-3 and PARP
Author Affiliations & Notes
  • X Zhang
    Ophthalmology
    Columbia University New York NY
  • GR Barile
    Ophthalmology
    Columbia University New York NY
  • S Pachydaki
    Ophthalmology
    Columbia University New York NY
  • D Liu
    Pathology
    Columbia University New York NY
  • WM Schiff
    Ophthalmology
    Columbia University New York NY
  • JR Sparrow
    Ophthalmology
    Columbia University New York NY
  • S Chang
    Ophthalmology
    Columbia University New York NY
  • Footnotes
    Commercial Relationships   X. Zhang, None; G.R. Barile, None; S. Pachydaki, None; D. Liu, None; W.M. Schiff, None; J.R. Sparrow, None; S. Chang, None. Grant Identification: Research to prevent blindness
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 3619. doi:
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    • Get Citation

      X Zhang, GR Barile, S Pachydaki, D Liu, WM Schiff, JR Sparrow, S Chang; Cell proliferation and Apoptosis in Vitreoretinal Disorders( PVR, PDR, Macular Pucker): Expression of Ki-67( MIB-1), PCNA, Cyclin E, CDK4, Caspase-3 and PARP . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3619.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: Inhibition of cell proliferation and induction of apoptosis have been implicated as potential therapeutic approaches for a variety of proliferative diseases such as proliferative vitreoretinopathy (PVR) and proliferative diabetic retinopathy(PDR) .The objectives of the present study are to assess the incidence of cell proliferation and apoptosis and further investigate the potential involvement of key regulators of cell cycle and apoptosis in epiretinal membranes(ERMs). Methods: ERMs were obtained from 23 eyes of 23 patients who underwent vitrectomy surgery for PVR, PDR and macular pucker(MP). Cell proliferation was evaluated by Ki-67 and PCNA (proliferation cell nuclear antigen) immunochemistry staining. Apoptosis was assessed by TUNEL assay. The expression of cyclin E, CDK4(cyclin-dependent kinase 4),caspase-3 and PARP(poly-ADP-ribose-polymerase) were detected using specific antibodies for cyclin E(M-20), CDK4(C-22), activated caspase-3 and p85 fragment of PARP. Cytokeratin and active caspase-3/PARP double staining was applied to localize RPE cells undergoing apoptosis. Results: The expression of Ki-67 and PCNA was detected in all the patients and appeared to be correlated with cyclin E and CDK4 expression. There were no significant differences in proliferative index(PI) between PVR and PDR(P=0.1682), PVR and MP (P=0.5380), PDR and MP(P=0.8330). The Ki-67 and PCNA expression occurs in RPE cells and/or glial cells. Apoptotic nuclei was correlated with the increased expression of activated caspase-3 and the p85 fragment of PARP. Most apoptotic cells appeared to be RPE cells. Apoptotic nuclei appeared to be presented more frequently in longstanding ERMs. However, no significant differences in apoptotic index(AI) were found between PVR and PDR(P=0.4828), PDR and MP(P=0.5492), PVR and MP(P=0.2144). Conclusions: This study supports the notion that cell proliferation and apoptosis are key regulatory mechanisms of specific cell population of ERMs in patients with PVR, PDR and macular pucker. Inhibition of cell cycle G1 regulators and induction of apoptotic regulators such as caspase-3 activation may serve therapeutic interventions for proliferative retinal disorders.

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