期刊
NEUROSCIENCE LETTERS
卷 520, 期 1, 页码 115-120出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2012.05.048
关键词
Amyotrophic lateral sclerosis; Superoxide dismutase; CD44; Neurodegeneration; Astrocyte; Microglia
资金
- Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of Japan [23110002]
- MEXT [18390099, 20390092]
- Ministry of Health, Labor, and Welfare of Japan (Health Sciences Research Grant on Comprehensive Research on Disability Health and Welfare [H21-012]
- Global COE program, MEXT
- Grants-in-Aid for Scientific Research [18390099, 20390092] Funding Source: KAKEN
Amyotrophic lateral sclerosis (ALS) is a motor neuron-specific neurodegenerative disease. An increasing body of evidence suggests that, in addition to cell autonomous regulation, i.e., pathological changes in motor neurons, non-cell autonomous mechanisms involving glial cells play critical roles in the pathogenesis of ALS. CD44 functions as a receptor for osteopontin and hyaluronan, and has been implicated in inflammation associated with neuronal injuries. However, this membrane glycoprotein has been poorly studied in ALS. Here we investigated its expression during ALS progression using SOD1(G93A) mice. CD44 expression increased around the onset of disease and then increased continuously. Astrocytes and microglia expressed CD44 in vivo. Consistent with these findings, primary cultured microglia began to express CD44 upon activation with LPS and interferon-gamma. CD44 expression in primary cultured astrocytes was also enhanced by activation with interferon-gamma+TNF-alpha or bFGF alone. As CD44 was detected in cell lysate, but not in culture media of astrocytes and microglia, it was likely that these glial cells expressed a membrane-bound form of CD44. Our study demonstrates that CD44 expression in astrocytes and microglia is closely associated with the pathogenesis of ALS, and suggests that inflammatory responses involving CD44 may play a role in this disease. (c) 2012 Elsevier Ireland Ltd. All rights reserved.
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