Laboratories

Department of Functional Anatomy and Neuroscience

KEYWORDS

  • Nerve injury
  • Nerve degeneration
  • Stress
  • Nerve regeneration Nerve degeneration
  • Amyotrophic lateral sclerosis
  • Alzheimer’s disease
  • Neuron
  • Glia
  • Organelle dynamics
  • Neuroinflammation

HEAD

KIRYU-SEO Sumiko

Professor

Researchers

LAB MEMBER

Faculty Position Researchers
NAGATA Kenichi Lecturer Researchers
MATSUMOTO Sakiko Lecturer Researchers
WAKATSUKI Koji Assistant professor Researchers

CONTACT

Email kaibou2◎med.nagoya-u.ac.jp (Please send a message after replacing "◎" mark with "@" mark. )
HP Private Page

OUTLINE

Nerve injury, neurodegenerative disease, aging, or stress significantly impair the function of the brain. They cause neuronal damage and consequently neuronal degeneration. Our laboratory aims to understand the fundamental mechanisms by which neurons and their surrounding cells respond to damage, using unique animal models. We believe that this basic research will lead to therapeutics and drug discovery that can prevent neuronal degeneration caused by injury or disease. Additionally, we are interested in the mechanism of the nerve dependent tissue repair. Nerves are abundantly distributed in the peripheral organs. When a peripheral organ is injured by damage or disease, the distributed nerves are also injured. Damaged nerves actively regulate the tissue repair: dysfunction in this process can lead to chronic disease and neurodegeneration. Our goal is to define the molecular mechanisms of the neuronal damage responses and elucidate disease pathophysiology using a unique approach with cutting-edge technologies, such as histological analysis, molecular biological analysis, omics analysis, and imaging analyses.

For more information about our research, please visit our laboratory's own website (https://www.med.nagoya-u.ac.jp/Anatomy2/).

RESEARCH PROJECTS

Major research topics include the following

1. The mechanism of neuronal damage response

  • Protein and organelle homeostasis and disruption in damaged neurons
  • Regulation of the damaged microenvironment in neurodegenerative diseases
  • The change of neuronal damage response in aging

2. erve-dependent mechanisms that promote repair of damaged organs and tissues

  • Nerve-dependent wound healing mechanisms
  • Neural circuits involved in chronic stress and their molecular mechanisms

BIBLIOGRAPHY

2025
  1. Tra T, Kiryu-Seo S, Kida H, Wakatsuki K, Tashiro Y, Tsutsumi M, Ataka M, Iguchi Y, Nemoto T, Takahashi R, Katsuno M, Kiyama H. Absence of the axon initial segment in sensory neuron enhances resistance to amyotrophic lateral sclerosis. Brain, 148(11), 4030-4044, 2025.
2024
  1. Wakatsuki K, Kiryu-Seo S, Yasui M, Yokota H, Kida H, Konishi H, Kiyama H. Repeated cold stress, an animal model for fibromyalgia, elicits proprioceptor-induced chronic pain with microglial activation in mice. J Neuroinflammation, 21(1), 25, 2024.
2022
  1. Kiryu-Seo S, Matsushita R, Tashiro R, Yoshimura T, Iguchi Y, Katsuno M, Ryosuke Takahashi R, Kiyama H. Impaired disassembly of the axon initial segment restricts mitochondrial entry into damaged axons. EMBO J, 41, e110486, 2022.
  2. Jin M, Matsumoto S, Ayaki T, Yamakado H, Taguchi T, Togawa N, Konno A, Hirai H, Nakajima H, Komai S, Ishida R, Chiba S, Takahashi R, Takao T, Hirotsune S. DOPAnization of tyrosine in α-synuclein by tyrosine hydroxylase leads to the formation of oligomers. Nat Commun 13(1) 6880, 2022.
2018
  1. Nagata K, Takahashi M, Matsuba Y, Okuyama-Uchimura F, Sato K, Hashimoto S, Saito T, Saido TC. Generation of App knock-in mice reveals deletion mutations protective against Alzheimer’s disease-like pathology. Nat Commun 9(1) 1800, 2018.
2017
  1. Kaneko A, Kiryu-Seo S, Matsumoto S, Kiyama H. Damage-induced neuronal endopeptidase (DINE) enhances axonal regeneration potential of retinal ganglion cells after optic nerve injury. Cell Death Dis, 8, e2847, 2017.
2016
  1. Nagata K, Kiryu-Seo S, Tamada H, Okuyama-Uchimura F, Kiyama H, Saido TC. ECEL1 mutation implicates impaired axonal arborization of motor nerves in the pathogenesis of distal arthrogryposis. Acta Neuropathol, 132, 111-126, 2016.
  2. Matsumoto S, Kiryu-Seo S, Kiyama H. Motor nerve arborization requires proteolytic domain of Damage-induced neuronal endopeptidase (DINE) during development. J Neurosci, 36, 4744-4757, 2016.
  3. Kiryu-Seo S, Tamada H, Kato Y, Yasuda K, Ishihara N, Nomura M, Mihara K, Kiyama H. Mitochondrial fission is an acute and adaptive response in injured motor neurons. Sci Rep, 6, 28331, 2016.
2000
  1. Kiryu-Seo S, Sasaki M, Yokohama H, Nakagomi S, Hirayama T, Aoki S, Wada K, Kiyama H. Damage induced neuronal endopeptidase (DINE) is a unique metallopeptidase expressed in response to neuronal damage and activates superoxide scavengers. Proc. Natl. Acad. Sci. USA. 2000; 97(8):4345-50.

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