ArticleMolecular medicine reports2019
Overexpression of COX6B1 protects against I/R‑induced neuronal injury in rat hippocampal neurons.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 19 citations in OpenAlex.
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4 authors at 2 institutions in 1 country.
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Abstract
Cerebrovascular disease (CVD) is one of the leading causes of mortality worldwide. The role of cytochrome c oxidase subunit 6B1 (COX6B1) in the central nervous system remains unclear. The present study aimed to analyze the role of COX6B1 in rat hippocampal neurons extracted from fetal rats. The subcellular localization of the neuron‑specific marker microtubule‑associated protein 2 was detected by immunofluorescence assay. Cell viability was assessed using a cell counting kit, and the levels of apoptosis and cytosolic Ca2+ were analyzed by flow cytometry. The expression levels of the molecular factors downstream to COX6B1 were determined using reverse transcription‑quantitative polymerase chain reaction and western blotting. Reoxygenation following oxygen‑glucose deprivation (OGD) decreased cell viability and the expression levels of COX6B1 in a time‑dependent manner, and 60 min of reoxygenation was identified as the optimal time period for establishing an ischemia/reperfusion (I/R) model. Overexpression of COX6B1 was demonstrated to reverse the viability of hippocampal neurons following I/R treatment. Specifically, COX6B1 overexpression decreased the cytosolic concentration of Ca2+ and suppressed neuronal apoptosis, which were increased following I/R treatment. Furthermore, overexpression of COX6B1 increased the protein expression levels of apoptosis regulator BCL‑2 and mitochondrial cytochrome c (cyt c), and decreased the protein expression levels of apoptosis regulator BCL2‑associated X and cytosolic cyt c in I/R model cells. Collectively, the present study results suggested that COX6B1 overexpression may reverse I/R‑induced neuronal damage by increasing the viability of neurons, by decreasing the cytosolic levels of Ca2+ and by suppressing apoptosis. These results may facilitate the development of novel strategies for the prevention and treatment of CVD.
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