July 2019
Volume 60, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2019
Beclin-1 is Not Stimulated During Development of Experimental Murine Cytomegalovirus (MCMV) Retinitis in Mice with Retrovirus-Induced Immunosuppression (MAIDS)
Author Affiliations & Notes
  • Judee Grace Nemeño
    Georgia State University, Atlanta, Georgia, United States
  • Jessica Carter
    Georgia State University, Atlanta, Georgia, United States
    Ophthalmology, Emory University, Georgia, United States
  • Richard D Dix
    Georgia State University, Atlanta, Georgia, United States
    Ophthalmology, Emory University, Georgia, United States
  • Footnotes
    Commercial Relationships   Judee Grace Nemeño, None; Jessica Carter, None; Richard Dix, None
  • Footnotes
    Support  NIH/NEI Grant EY010568, NIH/NEI Grant EY024630, NIH/NEI Core Grant P30/EY006360, Emory Eye Center Vision Training Grant NIH/NEI 5T32/EY007092-32, Research to Prevent Blindness, Fight for Sight
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 780. doi:
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    • Get Citation

      Judee Grace Nemeño, Jessica Carter, Richard D Dix; Beclin-1 is Not Stimulated During Development of Experimental Murine Cytomegalovirus (MCMV) Retinitis in Mice with Retrovirus-Induced Immunosuppression (MAIDS). Invest. Ophthalmol. Vis. Sci. 2019;60(9):780.

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

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Abstract

Purpose : We have been investigating the potential roles of several cell death pathways in the pathophysiology of AIDS-related human cytomegalovirus retinitis using a mouse model of MCMV retinitis in mice with MAIDS. Autophagy is a protective form of cell death induced during periods of stress. Previous work by others has shown autophagy to play an important role in the homeostasis of RPE, but MCMV may possess a mechanism during active replication to inhibit a late stage of autophagy in RPE. Because beclin-1 has a central role in autophagy, we tested the hypothesis that beclin-1, as a marker for autophagy, is downregulated during onset and development of MAIDS-related MCMV retinitis.

Methods : We have shown previously that mice with MAIDS of 4-weeks duration are resistant to MCMV retinitis, but mice with MAIDS of 10 weeks duration are susceptible to MCMV retinitis. The left eyes of groups of C57BL/6 mice with MAIDS-4 or MAIDS-10 were injected subretinally with MCMV. Right eyes were injected with maintenance medium only (control). At 3, 6, and 10 days postinfection, all eyes were collected and subjected to RT-PCR assay for detection and quantification of beclin-1 mRNA.

Results : Beclin-1 mRNA was detected but not stimulated nor downregulated within MCMV-infected eyes of MAIDS-4 mice resistant to retinitis at 3, 6, and 10 days postinfection. Similarly, MCMV-infected eyes of MAIDS-10 mice susceptible to retinitis showed detectable beclin-1 mRNA but without stimulation nor downregulation at all days postinfection investigated, even at 10 days postinfection at time of retinitis development.

Conclusions : MCMV infection of eyes of retinitis-resistant MAIDS-4 mice as well as retinitis-susceptible MAIDS-10 mice showed neither stimulation nor downregulation of beclin-1 mRNA. These preliminary findings suggest that autophagy may not play a prominent role in the development of MAIDS-related MCMV retinitis. Future studies will investigate the fate of other autophagy-related molecules during development of MCMV retinitis in mice with MAIDS. It has not escaped our attention that caspase-mediated cleavage of beclin-1 promotes crosstalk between apoptosis and autophagy.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.

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