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http://purl.uniprot.org/citations/25101006http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25101006http://www.w3.org/2000/01/rdf-schema#comment"

Background and aims

AIF (apoptosis inducing factor) is a flavin and NADH containing protein located within mitochondria required for optimal function of the respiratory chain. AIF may function as an antioxidant within mitochondria, yet when released from mitochondria it activates caspase-independent cell death. The Harlequin (Hq) mouse has a markedly reduced content of AIF, providing an experimental model to query if the main role of AIF in the exacerbation of cell death is enhanced mitochondrial generation of reactive oxygen species (ROS) or the activation of cell death programs. We asked if the ROS generation is altered in Hq heart mitochondria at baseline or following ischemia-reperfusion (IR).

Methods

Buffer perfused mouse hearts underwent 30 min ischemia and 30 min reperfusion. Mitochondrial function including oxidative phosphorylation and H2O2 generation was measured. Immunoblotting was used to determine the contents of AIF and PAR [poly(ADP-ribose)] in cell fractions.

Results

There were no differences in the release of H2O2 between wild type (WT) and Hq heart mitochondria at baseline. IR increased H2O2 generation from WT but not from Hq mitochondria compared to corresponding time controls. The complex I activity was decreased in WT but not in Hq mice following IR. The relocation of AIF from mitochondria to nucleus was increased in WT but not in Hq mice. IR activated PARP-1 only in WT mice. Cell injury was decreased in the Hq mouse heart following in vitro IR.

Conclusion

A deficiency of AIF within mitochondria does not increase ROS production during IR, indicating that AIF functions less as an antioxidant within mitochondria. The decreased cardiac injury in Hq mouse heart accompanied by less AIF translocation to the nucleus suggests that AIF relocation, rather than the AIF content within mitochondria, contributes to cardiac injury during IR."xsd:string
http://purl.uniprot.org/citations/25101006http://purl.org/dc/terms/identifier"doi:10.3389/fphys.2014.00271"xsd:string
http://purl.uniprot.org/citations/25101006http://purl.uniprot.org/core/author"Chen Q."xsd:string
http://purl.uniprot.org/citations/25101006http://purl.uniprot.org/core/author"Hu Y."xsd:string
http://purl.uniprot.org/citations/25101006http://purl.uniprot.org/core/author"Thompson J."xsd:string
http://purl.uniprot.org/citations/25101006http://purl.uniprot.org/core/author"Lesnefsky E.J."xsd:string
http://purl.uniprot.org/citations/25101006http://purl.uniprot.org/core/author"Szczepanek K."xsd:string
http://purl.uniprot.org/citations/25101006http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/25101006http://purl.uniprot.org/core/name"Front Physiol"xsd:string
http://purl.uniprot.org/citations/25101006http://purl.uniprot.org/core/pages"271"xsd:string
http://purl.uniprot.org/citations/25101006http://purl.uniprot.org/core/title"A deficiency of apoptosis inducing factor (AIF) in Harlequin mouse heart mitochondria paradoxically reduces ROS generation during ischemia-reperfusion."xsd:string
http://purl.uniprot.org/citations/25101006http://purl.uniprot.org/core/volume"5"xsd:string
http://purl.uniprot.org/citations/25101006http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25101006
http://purl.uniprot.org/citations/25101006http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/25101006
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http://purl.uniprot.org/uniprot/#_Q9Z0X1-mappedCitation-25101006http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25101006
http://purl.uniprot.org/uniprot/Q9Z0X1http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25101006
http://purl.uniprot.org/uniprot/B1AU25http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25101006