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http://purl.uniprot.org/citations/25017576http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25017576http://www.w3.org/2000/01/rdf-schema#comment"Cerebral ischemia/reperfusion (I/R) can induce neuronal death, particularly in the hippocampal formation (HF). Molecular genetic studies have suggested that the activities of the transcription factor, hypoxia-inducible factor-1α (HIF-1α), are closely linked to ischemia-induced neuronal death. However, the mechanisms through which HIF-1α functions remain poorly understood. In this study, primary cortical neurons were subjected to oxygen‑glucose deprivation (OGD) to establish a cell model of OGD/reperfusion (RP). HIF-1α mRNA and protein expression was measured by qRT-PCR and western blot analysis. Cell proliferation was detected by MTT assay. Flow cytometric analysis was used to detect cell apoptosis and changes in mitochondrial mass. The expression of LC3-Ⅰ and LC3-Ⅱ was examined by western blot analysis. We found that HIF-1α increased cell proliferation and decreased cell apoptosis in our cell model of OGD/RP using cultured neonatal rat cortical neurons. The overexpression of HIF-1α significantly induced changes in mitochondrial mass and mitochondrial autophagy in cortical neurons. Moreover, the inhibition of HIF-1α markedly suppressed cell proliferation and mitochondrial autophagy. We also demonstrated that the HIF-1α-induced mitochondrial autophagy was accompanied by the inhibition of the mTOR pathway. This study provides direct in vitro evidence that HIF-1α overexpression triggers mitochondrial autophagy, thereby increasing neuronal survival. Our results highlight a novel target molecule toward which anti-ischemic neuroprotective effects can be applied."xsd:string
http://purl.uniprot.org/citations/25017576http://purl.org/dc/terms/identifier"doi:10.3892/ijmm.2014.1850"xsd:string
http://purl.uniprot.org/citations/25017576http://purl.uniprot.org/core/author"Dai X."xsd:string
http://purl.uniprot.org/citations/25017576http://purl.uniprot.org/core/author"Hou L."xsd:string
http://purl.uniprot.org/citations/25017576http://purl.uniprot.org/core/author"Liu Y."xsd:string
http://purl.uniprot.org/citations/25017576http://purl.uniprot.org/core/author"Sun Y."xsd:string
http://purl.uniprot.org/citations/25017576http://purl.uniprot.org/core/author"Wang X."xsd:string
http://purl.uniprot.org/citations/25017576http://purl.uniprot.org/core/author"Hu L."xsd:string
http://purl.uniprot.org/citations/25017576http://purl.uniprot.org/core/author"Yin L."xsd:string
http://purl.uniprot.org/citations/25017576http://purl.uniprot.org/core/author"Bai S."xsd:string
http://purl.uniprot.org/citations/25017576http://purl.uniprot.org/core/author"Gong G."xsd:string
http://purl.uniprot.org/citations/25017576http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/25017576http://purl.uniprot.org/core/name"Int J Mol Med"xsd:string
http://purl.uniprot.org/citations/25017576http://purl.uniprot.org/core/pages"1133-1140"xsd:string
http://purl.uniprot.org/citations/25017576http://purl.uniprot.org/core/title"Upregulation of HIF-1alpha protein induces mitochondrial autophagy in primary cortical cell cultures through the inhibition of the mTOR pathway."xsd:string
http://purl.uniprot.org/citations/25017576http://purl.uniprot.org/core/volume"34"xsd:string
http://purl.uniprot.org/citations/25017576http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25017576
http://purl.uniprot.org/citations/25017576http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/25017576
http://purl.uniprot.org/uniprot/#_A6HC66-mappedCitation-25017576http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25017576
http://purl.uniprot.org/uniprot/#_A6HC67-mappedCitation-25017576http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25017576
http://purl.uniprot.org/uniprot/#_A6IU70-mappedCitation-25017576http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25017576
http://purl.uniprot.org/uniprot/#_P42346-mappedCitation-25017576http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25017576
http://purl.uniprot.org/uniprot/#_O35800-mappedCitation-25017576http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25017576
http://purl.uniprot.org/uniprot/A6HC66http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25017576