June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Retinal circadian clock modulates cone photoreceptor viability in mice
Author Affiliations & Notes
  • Kenkichi Baba
    Morehouse School of Medicine, Atlanta, Georgia, United States
  • Ilaria Piano
    Università di Pisa, Pisa, Italy
  • Glaudia Gargini
    Università di Pisa, Pisa, Italy
  • P. Michael Iuvone
    Emory University, Atlanta, Georgia, United States
  • Gianluca Tosini
    Morehouse School of Medicine, Atlanta, Georgia, United States
  • Footnotes
    Commercial Relationships   Kenkichi Baba, None; Ilaria Piano, None; Glaudia Gargini, None; P. Michael Iuvone, None; Gianluca Tosini, None
  • Footnotes
    Support  NIH Grant GM116760 to K.B., R01EY004864, P30EY006360, Research to Prevent Blindness to P.M.I., R01EY026291 to G.T.
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 4141. doi:
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      Kenkichi Baba, Ilaria Piano, Glaudia Gargini, P. Michael Iuvone, Gianluca Tosini; Retinal circadian clock modulates cone photoreceptor viability in mice. Invest. Ophthalmol. Vis. Sci. 2017;58(8):4141.

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

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Purpose : The widespread control of signaling, metabolism, and gene expression exerted by the ocular circadian clocks suggests that the molecular clockworks, or their output signals, may contribute to ocular disease and pathology as well as to normal visual function. For example, signaling by the retinal clock and its outputs seem to play a role in the regulation of eye growth and refractive errors. Furthermore, the mammalian retinal clock influences cell survival and growth processes in the eye, including the susceptibility of photoreceptors to degeneration from light damage. Bmal1 gene is a key component of the mammalian circadian clock. Bmal1 knock-out (KO) mice (Bmal1-/-) at young age do not show any circadian rhythmicity and develop several pathologies. Bmal1 KOs show premature aging and the lifespan is significantly reduced (about nine months). The purpose of our study is to investigate the role of Bmal1 removal on cone photoreceptor function and viability during aging using neural retina specific Bmal1 KO mice.

Methods : Photoreceptor viability was assessed in the retina of neural retina specific Bmal1 KO (Chx10Cre-Bmal1loxP/loxP) mice at young (3 month old) and old (26 month old) ages. The thickness of photoreceptors layers (PRL) was first assessed non-invasively using spectral domain optical coherence tomography (SD-OCT). The eyes of Chx10Cre-Bmal1loxP/loxP mice were subsequently explanted, and sectioned for immunohistochemical analysis. Chx10Cre mice were used as controls.

Results : SD-OCT analysis indicated that the PRL thickness of Chx10Cre-Bmal1loxP/loxP mice at 26 months of age is significantly reduced with respect to the PRL thickness of 3 month old Chx10Cre-Bmal1loxP/loxP or 26 month old controls. Our immunohistochemical analysis also revealed a significant reduction in the number of cone photoreceptors in 26 old months Chx10Cre-Bmal1loxP/loxP mice. Finally significant alterations in the circuitry of outer plexiform layer were observed not only in 26 months old Chx10Cre-Bmal1loxP/loxP, but also in 3 and 12 months old mice, indicating a possible defect in retinal development.

Conclusions : Our results indicate that removal of a functional circadian clock from the cones may affect the viability of these cells during aging and maybe affect the development of entire retinal structure.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.


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