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Haploinsufficiency in the mitochondrial protein CHCHD4 reduces brain injury in a mouse model of neonatal hypoxia-ischemia

Artikel i vetenskaplig tidskrift
Författare Yanyan Sun
Tao Li
Cuicui Xie
Yiran Xu
Kai Zhou
Juan Rodriguez
Wei Han
Xiaoyang Wang
G. Kroemer
N. Modjtahedi
K. Blomgren
Changlian Zhu
Publicerad i Cell Death & Disease
Volym 8
ISSN 2041-4889
Publiceringsår 2017
Publicerad vid Institutionen för neurovetenskap och fysiologi
Språk en
Länkar dx.doi.org/10.1038/cddis.2017.196
Ämnesord APOPTOSIS-INDUCING FACTOR, RECOMBINANT-HUMAN-ERYTHROPOIETIN, FOCAL, CEREBRAL-ISCHEMIA, NEURONAL CELL-DEATH, INTERMEMBRANE SPACE, PRETERM, INFANTS, CYTOCHROME-C, P53, NEUROPROTECTION, TRANSLOCATION
Ämneskategorier Neurovetenskaper, Cellbiologi

Sammanfattning

Mitochondria contribute to neonatal hypoxic-ischemic brain injury by releasing potentially toxic proteins into the cytosol. CHCHD4 is a mitochondrial intermembrane space protein that plays a major role in the import of intermembrane proteins and physically interacts with apoptosis-inducing factor (AIF). The purpose of this study was to investigate the impact of CHCHD4 haploinsufficiency on mitochondrial function and brain injury after cerebral hypoxia-ischemia (HI) in neonatal mice. CHCHD4(+/-) and wild-type littermate mouse pups were subjected to unilateral cerebral HI on postnatal day 9. CHCHD4 haploinsufficiency reduced insult-related AIF and superoxide dismutase 2 release from the mitochondria and reduced neuronal cell death. The total brain injury volume was reduced by 21.5% at 3 days and by 31.3% at 4 weeks after HI in CHCHD4(+/-) mice. However, CHCHD4 haploinsufficiency had no influence on mitochondrial biogenesis, fusion, or fission; neural stem cell proliferation; or neural progenitor cell differentiation. There were no significant changes in the expression or distribution of p53 protein or p53 pathway-related genes under physiological conditions or after HI. These results suggest that CHCHD4 haploinsufficiency afforded persistent neuroprotection related to reduced release of mitochondrial intermembrane space proteins. The CHCHD4-dependent import pathway might thus be a potential therapeutic target for preventing or treating neonatal brain injury.

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