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Lack of the brain-specific isoform of apoptosis-inducing factor aggravates cerebral damage in a model of neonatal hypoxia-ischemia.

Journal article
Authors Juan Rodriguez
Yaodong Zhang
Tao Li
Cuicui Xie
Yanyan Sun
Yiran Xu
Kai Zhou
Kaiming Huo
Yafeng Wang
Xiaoyang Wang
Daniel Andersson
Anders Ståhlberg
Qinghe Xing
Carina Mallard
Henrik Hagberg
Nazanine Modjtahedi
Guido Kroemer
Klas Blomgren
Changlian Zhu
Published in Cell death & disease
Volume 10
Issue 1
Pages 3
ISSN 2041-4889
Publication year 2018
Published at Institute of Neuroscience and Physiology
Institute of Biomedicine, Department of Pathology
Institute of Clinical Sciences, Department of Obstetrics and Gynecology
Pages 3
Language en
Subject categories Neurosciences


Apoptosis-inducing factor (AIF) may contribute to neuronal cell death, and its influence is particularly prominent in the immature brain after hypoxia-ischemia (HI). A brain-specific AIF splice-isoform (AIF2) has recently been discovered, but has not yet been characterized at the genetic level. The aim of this study was to determine the functional and regulatory profile of AIF2 under physiological conditions and after HI in mice. We generated AIF2 knockout (KO) mice by removing the AIF2-specific exon and found that the relative expression of Aif1 mRNA increased in Aif2 KO mice and that this increase became even more pronounced as Aif2 KO mice aged compared to their wild-type (WT) littermates. Mitochondrial morphology and function, reproductive function, and behavior showed no differences between WT and Aif2 KO mice. However, lack of AIF2 enhanced brain injury in neonatal mice after HI compared to WT controls, and this effect was linked to increased oxidative stress but not to caspase-dependent or -independent apoptosis pathways. These results indicate that AIF2 deficiency exacerbates free radical production and HI-induced neonatal brain injury.

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