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Neuroprotection by selective neuronal deletion of Atg7 in neonatal brain injury

Journal article
Authors Cuicui Xie
V. Ginet
Yanyan Sun
M. Koike
Kai Zhou
Tao Li
Hongfu Li
Qian Li
Xiaoyang Wang
Y. Uchiyama
A. C. Truttmann
G. Kroemer
J. Puyal
K. Blomgren
Changlian Zhu
Published in Autophagy
Volume 12
Issue 2
Pages 410-423
ISSN 1554-8627
Publication year 2016
Published at Institute of Neuroscience and Physiology
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Pages 410-423
Language en
Keywords apoptosis, ATG7, autophagy, caspase, hypoxic-ischemic encephalopathy, newborn, cerebral hypoxia-ischemia, apoptosis-inducing factor, cell-death, rat, model, autophagy, activation, outcomes, encephalopathy, involvement, inhibition
Subject categories Clinical Medicine


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.

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