Our previous study demonstrated that adenovirus-delivered GFP nuclear heme oxygenase-1 (nuclear HO-1, NHO-1) fragments lacking 23 amino acids at the C-terminus (Ad-GFP-HO-1C[INCREMENT]23) showed the potential therapeutic effects mediated by its improvement of the blood-spinal cord barrier (BSCB) integrity. However, the NHO-1-mediated molecular mechanism in regulating the BSCB function remains unclear. The BSCB model in vitro was established via a coculture of primary rat brain microvascular endothelial cells (RBMECs) and spinal cord astrocytes on transwell system.
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