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Yusuke Murakami Last modified date：2020.06.06

Lecturer / Ophthalmology
Kyushu University Hospital




Homepage
https://kyushu-u.pure.elsevier.com/en/persons/yusuke-murakami
　Reseacher Profiling Tool　Kyushu University Pure
Phone
092-642-5648
Fax
092-642-5663
Academic Degree
M.D., Ph.D.
Field of Specialization
Retina degenerative diseases, Glaucoma
Research
Research Interests
  • Structure- function relationships and their association with genotypes in retinitis pigmentosa
    keyword : Structure-function relationships
    2020.04～2024.03.
  • Development of regenerative medicine in retinal and optic nerve degeneration
    keyword : Regeneration
    2018.04～2022.03.
  • Regulation of chronic inflammation in retinal/optic nerve degeneration and development of novel therapeutics
    keyword : Neuroinflammation
    2015.04～2020.03.
  • Development of novel therapeutics in retinal degenerative diseases
    keyword : Cell death
    2015.01～2018.03.
  • Clinical trials of neuroprotective gene therapy for patietns with retinitis pigmentosa
    keyword : Gene therapy
    2019.03～2022.03.
Academic Activities
Reports
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Papers
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1. Shunji Nakatake, yusuke murakami, Yasuhiro Ikeda, Noriko Morioka, Takashi Tachibana, Kohta Fujiwara, Noriko Yoshida, Shoji Notomi, Toshio Hisatomi, Shigeo Yoshida, Tatsuro Ishibashi, Yusaku Nakabeppu, Kohei Sonoda, MUTYH promotes oxidative microglial activation and inherited retinal degeneration, JCI insight, 1, 15, e87781, 2016.09, Oxidative stress is implicated in various neurodegenerative disorders, including retinitis pigmentosa (RP), an inherited disease that causes blindness. The biological and cellular mechanisms by which oxidative stress mediates neuronal cell death are largely unknown. In a mouse model of RP (rd10 mice), we show that oxidative DNA damage activates microglia through MutY homolog-mediated (MUYTH-mediated) base excision repair (BER), thereby exacerbating retinal inflammation and degeneration. In the early stage of retinal degeneration, oxidative DNA damage accumulated in the microglia and caused single-strand breaks (SSBs) and poly(ADP-ribose) polymerase activation. In contrast, Mutyh deficiency in rd10 mice prevented SSB formation in microglia, which in turn suppressed microglial activation and photoreceptor cell death. Moreover, Mutyh-deficient primary microglial cells attenuated the polarization to the inflammatory and cytotoxic phenotype under oxidative stress. Thus, MUTYH-mediated BER in oxidative microglial activation may be a novel target to dampen the disease progression in RP and other neurodegenerative disorders that are associated with oxidative stress..
Presentations
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Awards
  • Association between inflammation and cone cell loss in retinitis pigmentosa


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