Version 1
: Received: 1 November 2023 / Approved: 1 November 2023 / Online: 1 November 2023 (13:26:24 CET)
How to cite:
Funaki, M.; Nio-Kobayashi, J.; Suzuki, R.; Bando, Y. Implication of Galectin-3 for Neuroinflammation in the Visual Pathway of the Experimental Optic Neuritis. Preprints2023, 2023110095. https://doi.org/10.20944/preprints202311.0095.v1
Funaki, M.; Nio-Kobayashi, J.; Suzuki, R.; Bando, Y. Implication of Galectin-3 for Neuroinflammation in the Visual Pathway of the Experimental Optic Neuritis. Preprints 2023, 2023110095. https://doi.org/10.20944/preprints202311.0095.v1
Funaki, M.; Nio-Kobayashi, J.; Suzuki, R.; Bando, Y. Implication of Galectin-3 for Neuroinflammation in the Visual Pathway of the Experimental Optic Neuritis. Preprints2023, 2023110095. https://doi.org/10.20944/preprints202311.0095.v1
APA Style
Funaki, M., Nio-Kobayashi, J., Suzuki, R., & Bando, Y. (2023). Implication of Galectin-3 for Neuroinflammation in the Visual Pathway of the Experimental Optic Neuritis. Preprints. https://doi.org/10.20944/preprints202311.0095.v1
Chicago/Turabian Style
Funaki, M., Ryoji Suzuki and Yoshio Bando. 2023 "Implication of Galectin-3 for Neuroinflammation in the Visual Pathway of the Experimental Optic Neuritis" Preprints. https://doi.org/10.20944/preprints202311.0095.v1
Abstract
Although multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) that results in many neurological disabilities, optic neuritis (ON) is developed in some MS patients. However, the molecular mechanism of ON remains unknown. Galectins, β-galactoside-binding lectins, are involved in various pathophysiology. We have previously shown that galectin-3 (gal-3) is associated with the pathogenesis of experimental autoimmune encephalomyelitis (EAE), its animal model for human MS. In the current study, the expression of gal-3 was explored in the visual pathway of the EAE mice to clarify the pathogenesis of ON.
Immunohistochemical analysis demonstrated that expression of gal-3 was increased in the visual pathway of the EAE mice during the peak disease, compared with naïve and EAE mice during the chronic disease. Expression of gal-3 was observed in mainly microglia/macrophages and astrocytes in the visual pathway of the EAE mice. In addition, gal-3+Iba-1+ cells with the phagocytic activities reflected by immunostaining with cathepsin-D were accumulated at demyelinating lesions in the visual pathway during peak disease of EAE. Moreover, NLRP3 expression was also detected in most gal-3+Iba-1+ cells. These results indicate a considerable possibility that gal-3 regulates the NLRP3 signaling in microglia/macrophages, followed by neuroinflammatory demyelination in ON. By contrast, astrocytic expression of gal-3 was also observed from the peak to the chronic disease. Taken together, the current study suggests a critical role of gal-3 in the pathogenesis of ON and proposes gal-3 in glial cells as a potential therapeutic target for ON.
Medicine and Pharmacology, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
