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<p>Spinal cord injury (SCI), which results in severe lower-limb motor dysfunction, is a neurological disorder that damages the central nervous system. Disruption of the blood–spinal cord barrier (BSCB) results in secondary injury and neuronal apoptosis. Thus, this study aimed to investigate the effect of nuclear heme oxygenase-1 (HO-1) on BSCB after hypoxia in an in vitro model and to identify the potential regulatory mechanism of nuclear HO-1 (nHO-1) in BSCB. In an in vitro hypoxia model, nHO-1 treatment attenuated BSCB permeability. In addition, western blot analysis indicated that the expression levels of tight junction–associated proteins (ZO-1, occludin) and adherens junction–associated proteins (VE-cadherin) increased after treatment with nHO-1. Reverse transcription quantitative PCR assay showed that the mRNA levels of these proteins were remarkable in cells overexpressing nHO-1. The immunofluorescence staining of ZO-1 showed a similar trend. Our data indicated that nHO-1 decreased the number of TUNEL-positive cells. Therefore, nHO-1 could decrease the permeability of the BSCB by promoting the protein expression levels of ZO-1, occludin, and VE-cadherin and by reducing the apoptosis of spinal cord microvascular endothelial cells. Our study provides new insights into the molecular mechanism by which nHO-1 regulates BSCB after SCI, demonstrating that nHO-1 may be a viable target for the treatment of SCI.</p>

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The protective role of nuclear Heme oxygenase-1 in blood-spinal cord barrier after hypoxia in vitro

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月2日

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  • Jian Wang,
  • Hui Wang,
  • Tingting Wang,
  • Po Zhang,
  • Yang Cao,
  • Tengbo Yu

摘要

Spinal cord injury (SCI), which results in severe lower-limb motor dysfunction, is a neurological disorder that damages the central nervous system. Disruption of the blood–spinal cord barrier (BSCB) results in secondary injury and neuronal apoptosis. Thus, this study aimed to investigate the effect of nuclear heme oxygenase-1 (HO-1) on BSCB after hypoxia in an in vitro model and to identify the potential regulatory mechanism of nuclear HO-1 (nHO-1) in BSCB. In an in vitro hypoxia model, nHO-1 treatment attenuated BSCB permeability. In addition, western blot analysis indicated that the expression levels of tight junction–associated proteins (ZO-1, occludin) and adherens junction–associated proteins (VE-cadherin) increased after treatment with nHO-1. Reverse transcription quantitative PCR assay showed that the mRNA levels of these proteins were remarkable in cells overexpressing nHO-1. The immunofluorescence staining of ZO-1 showed a similar trend. Our data indicated that nHO-1 decreased the number of TUNEL-positive cells. Therefore, nHO-1 could decrease the permeability of the BSCB by promoting the protein expression levels of ZO-1, occludin, and VE-cadherin and by reducing the apoptosis of spinal cord microvascular endothelial cells. Our study provides new insights into the molecular mechanism by which nHO-1 regulates BSCB after SCI, demonstrating that nHO-1 may be a viable target for the treatment of SCI.