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• W1574669501 abstract "Object Oxidative stress contributes to secondary injury after spinal cord injury (SCI). The expression of heme oxygenase-1 (HO-1), which protects cells from various insults including oxidative stress, is upregulated in injured spinal cords. Mice deficient in Bach1 (Bach1 −/− ), a transcriptional repressor of the HO-1 and beta-globin genes, express high levels of HO-1 mRNA and protein in various organs. The authors hypothesized that HO-1 modulates the secondary injury process after SCI in Bach1 −/− mice. Methods Male C57BL/6 (wild-type) and homozygous Bach1 −/− C57BL/6 mice were subjected to moderate SCI, and differences in hindlimb motor function, and electrophysiological, molecular biological, and histopathological changes were assessed for 2 weeks. Results Functional recovery was greater, and motor evoked potentials were significantly larger in Bach1 −/− mice than in wild-type mice throughout the observation period. The expression of HO-1 mRNA in the spinal cord was significantly increased in both mice until 3 days after injury, and it was significantly higher in Bach1 −/− mice than in wild-type mice at every assessment point. Histological examination using Luxol fast blue staining at 1 day after injury showed that the injured areas were smaller in Bach1 −/− mice than in wild-type mice. The HO-1 immunoreactivity was not detected in uninjured spinal cord, but 3 days postinjury the number of HO-1–immunoreactive cells was obviously higher in the injured area in both mice, particularly in Bach1 −/− mice. The HO-1 was primarily induced in microglia/macrophage in both mice. Conclusions These results suggest that HO-1 modulates the secondary injury process, and high HO-1 expression may preserve spinal cord function in the early stages after SCI in Bach1 −/− mice. Treatment that induces HO-1 expression at these early stages may preserve the functional outcome after SCI." @default.
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• W1574669501 date "2008-12-01" @default.
• W1574669501 modified "2023-09-26" @default.
• W1574669501 title "Modulation of the secondary injury process after spinal cord injury in Bach1-deficient mice by heme oxygenase–1" @default.
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• W1574669501 doi "https://doi.org/10.3171/spi.2008.10.08488" @default.
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