KMID : 1034820230190020353
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Molecular & Cellular Toxicology 2023 Volume.19 No. 2 p.353 ~ p.361
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Osteopontin promotes microglia activation and aggravates neuromyelitis optica via interferon-gamma/nuclear factor kappa B/interleukin-12 signaling
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Fengyi Chen
Yanping Wang
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Abstract
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Background : Neuromyelitis optica (NMO) is an inflammatory demyelinating disorder featured with the presence of serum aquaporin-4 immunoglobulin G antibodies (AQP4-IgG).
Objective : Osteopontin (OPN) was reported to be upregulated in NMO; however, the detailed function of OPN in NMO is obscure.
Results : Downregulation of OPN alleviated demyelination, axonal loss, microglia activation, neutrophil infiltration, inflammatory response and astrocyte apoptosis, but increased neurotrophic factor levels in murine spinal cords. Moreover, knockdown of OPN suppressed the expression of its downstream molecules, including interferon-gamma (IFN-¥ã), nuclear factor kappa B (NF-kB) and interleukin-12 (IL-12).
Conclusion : OPN promotes microglia activation and facilitates the pathogenesis of NMO by activating the IFN-¥ã/NF-kB/IL-12 signaling pathway.
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KEYWORD
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Neuromyelitis optica, Osteopontin, Microglia, Interferon-gamma and interleukin-12 signaling
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