June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Suppression of Drusen-like Deposits by a Novel VCP modulator in CCR2 Deficient Mice
Author Affiliations & Notes
  • Yuki Muraoka
    Ophthalmology & Visual Sciences, Kyoto University, Grad Sch of Med, Kyoto, Japan
  • Hanako Ohashi Ikeda
    Ophthalmology & Visual Sciences, Kyoto University, Grad Sch of Med, Kyoto, Japan
    Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital, Kyoto, Japan
  • Yuto Iida
    Ophthalmology & Visual Sciences, Kyoto University, Grad Sch of Med, Kyoto, Japan
  • Masayuki Hata
    Ophthalmology & Visual Sciences, Kyoto University, Grad Sch of Med, Kyoto, Japan
    Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital, Kyoto, Japan
  • tomoko hasegawa
    Ophthalmology & Visual Sciences, Kyoto University, Grad Sch of Med, Kyoto, Japan
  • Munemitsu Yoshikawa
    Ophthalmology & Visual Sciences, Kyoto University, Grad Sch of Med, Kyoto, Japan
  • Akira Kakizuka
    Laboratory of Functional Biology, Kyoto University Graduate School of Biostudies & Solution Oriented Research for Science and Technology, Kyoto, Japan
  • Nagahisa Yoshimura
    Ophthalmology & Visual Sciences, Kyoto University, Grad Sch of Med, Kyoto, Japan
  • Footnotes
    Commercial Relationships Yuki Muraoka, Kyoto University  (P); Hanako Ikeda, Kyoto University  (P); Yuto Iida, None; Masayuki Hata, None; tomoko hasegawa, None; Munemitsu Yoshikawa, None; Akira Kakizuka, Kyoto University  (P); Nagahisa Yoshimura, Canon (F), Kyoto University  (P), Nidek (C), Nidek (F), Topcon Corporation  (F)
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 2272. doi:
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      Yuki Muraoka, Hanako Ohashi Ikeda, Yuto Iida, Masayuki Hata, tomoko hasegawa, Munemitsu Yoshikawa, Akira Kakizuka, Nagahisa Yoshimura; Suppression of Drusen-like Deposits by a Novel VCP modulator in CCR2 Deficient Mice. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2272.

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

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Abstract

Purpose: VCP is a ubiquitously expressed ATPase that is reported to be involved in several physiological activities as well as neurodegeneration.1 In this study, we investigated whether our newly developed novel VCP modulator could resolve drusen-like deposits in eyes of older CCR2 deficient mice2 (experiment 1) or suppress deposit formation in eyes of younger CCR2 deficient mice (experiment 2).<br />

Methods: The mice were orally administered either a VCP modulator (Kyoto University Substance [KUS] group; n = 15) or saline (control group; n = 24) from the ages of 9 months and 2 months in experiments 1 and 2, respectively. Fundus photographs were used to determine the number of drusen-like deposits at each evaluation point.<br /> <br /> Ref.1) Kakizuka, A. Biochem. Soc. Trans. 2008: 36: 105-8.<br /> Ref.2) Ambati J et al. Nat Med. 2003;9:1390-7<br />

Results: Experiment 1: The number of deposits in the KUS group at 6 months of age (baseline) was similar to that observed in the control group (7.5 ± 9.8 and 10.3 ± 10.9, respectively). Although the deposits in the control group increased with age, those in the KUS group did not (100.7 ± 99.3 and 12.3 ± 22.1, respectively, at 15 months) and were significantly less in number than those in the control group from 11-15 months of age (P < 0.01). During observation, the number of deposits appeared to have decreased in the eyes of some mice in the KUS group.<br /> Experiment 2: The number of deposits in the control group was not significantly different from those in the KUS group at 2 months of age (baseline). The number of deposits in the control group increased with age, while those in the KUS group did not. At 9 months of age, the number of deposits in the KUS group was significantly lesser than those in the control group (4.4 ± 3.5 vs. 22.8 ± 28.5, respectively, P < 0.01).<br />

Conclusions: KUS, a novel VCP modulator, can be used to suppress the formation of drusen-like deposits in the eyes of CCR2 deficient mice.

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