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Göteborgs universitets publikationer

Neuroprotection by selective neuronal deletion of Atg7 in neonatal brain injury

Författare och institution:
Cuicui Xie (Institutionen för neurovetenskap och fysiologi); V. Ginet (-); Yanyan Sun (Institutionen för neurovetenskap och fysiologi); M. Koike (-); Kai Zhou (Institutionen för neurovetenskap och fysiologi); Tao Li (Institutionen för neurovetenskap och fysiologi); Hongfu Li (Institutionen för neurovetenskap och fysiologi); Qian Li (Institutionen för neurovetenskap och fysiologi); Xiaoyang Wang (Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering); Y. Uchiyama (-); A. C. Truttmann (-); G. Kroemer (-); J. Puyal (-); K. Blomgren (-); Changlian Zhu (Institutionen för neurovetenskap och fysiologi)
Publicerad i:
Autophagy, 12 ( 2 ) s. 410-423
Artikel, refereegranskad vetenskaplig
Sammanfattning (abstract):
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.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
Klinisk medicin
apoptosis, ATG7, autophagy, caspase, hypoxic-ischemic encephalopathy, newborn, cerebral hypoxia-ischemia, apoptosis-inducing factor, cell-death, rat, model, autophagy, activation, outcomes, encephalopathy, involvement, inhibition
Postens nummer:
Posten skapad:
2016-05-06 11:13
Posten ändrad:
2016-09-06 08:52

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