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  • Xie, CuicuiGothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology (author)

Neuroprotection by selective neuronal deletion of Atg7 in neonatal brain injury

  • Article/chapterEnglish2016

Publisher, publication year, extent ...

  • 2016-02-22
  • Informa UK Limited,2016

Numbers

  • LIBRIS-ID:oai:gup.ub.gu.se/236055
  • https://gup.ub.gu.se/publication/236055URI
  • https://doi.org/10.1080/15548627.2015.1132134DOI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:133334937URI

Supplementary language notes

  • Language:English

Part of subdatabase

Classification

  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • Perinatal asphyxia induces neuronal cell death and brain injury, and is often associated with irreversible neurological deficits in children. There is an urgent need to elucidate the neuronal death mechanisms occurring after neonatal hypoxia-ischemia (HI). We here investigated the selective neuronal deletion of the Atg7 (autophagy related 7) gene on neuronal cell death and brain injury in a mouse model of severe neonatal hypoxia-ischemia. Neuronal deletion of Atg7 prevented HI-induced autophagy, resulted in 42% decrease of tissue loss compared to wild-type mice after the insult, and reduced cell death in multiple brain regions, including apoptosis, as shown by decreased caspase-dependent and -independent cell death. Moreover, we investigated the lentiform nucleus of human newborns who died after severe perinatal asphyxia and found increased neuronal autophagy after severe hypoxic-ischemic encephalopathy compared to control uninjured brains, as indicated by the numbers of MAP1LC3B/LC3B (microtubule-associated protein 1 light chain 3)-, LAMP1 (lysosomal-associated membrane protein 1)-, and CTSD (cathepsin D)-positive cells. These findings reveal that selective neuronal deletion of Atg7 is strongly protective against neuronal death and overall brain injury occurring after HI and suggest that inhibition of HI-enhanced autophagy should be considered as a potential therapeutic target for the treatment of human newborns developing severe hypoxic-ischemic encephalopathy.

Subject headings and genre

Added entries (persons, corporate bodies, meetings, titles ...)

  • Ginet, V. (author)
  • Sun, YanyanGothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology(Swepub:gu)xsunyg (author)
  • Koike, M. (author)
  • Zhou, KaiKarolinska Institutet,Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology(Swepub:gu)xzhoka (author)
  • Li, TaoGothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology(Swepub:gu)xlitae (author)
  • Li, HongfuGothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology (author)
  • Li, Qian,1983Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology(Swepub:gu)xliqit (author)
  • Wang, Xiaoyang,1965Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation(Swepub:gu)xwanxi (author)
  • Uchiyama, Y. (author)
  • Truttmann, A. C. (author)
  • Kroemer, G. (author)
  • Puyal, J. (author)
  • Blomgren, K.Karolinska Institutet (author)
  • Zhu, Changlian,1964Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology(Swepub:gu)xzhuch (author)
  • Göteborgs universitetInstitutionen för neurovetenskap och fysiologi (creator_code:org_t)

Related titles

  • In:Autophagy: Informa UK Limited12:2, s. 410-4231554-86271554-8635

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