In:
Neurodegenerative Diseases, S. Karger AG, Vol. 6, No. 3 ( 2009), p. 118-126
Abstract:
〈 i 〉 Background: 〈 /i 〉 Neuroinflammation has been implicated in the pathomechanism of amyotrophic lateral sclerosis (ALS). It is known that signal transducer and activator of transcription-3 (STAT3) is a proinflammatory transcription factor. However, it remains to be determined whether STAT3 is involved in ALS. 〈 i 〉 Objective: 〈 /i 〉 To test the hypothesis that STAT3 may be upregulated, activated, or both in the spinal cord of ALS patients. 〈 i 〉 Methods: 〈 /i 〉 We performed immunohistochemical, immunoblot and densitometric analyses of total STAT3 (t-STAT3) or phosphorylated active form of STAT3 (p-STAT3) in spinal cords obtained at autopsy from 10 sporadic ALS patients and 10 age-matched control subjects. 〈 i 〉 Results: 〈 /i 〉 On sections, p-STAT3 immunoreactivity was localized in the nucleus as well as the cytoplasm of almost all activated microglia in the ALS cases, while it was detectable in a few resting microglia in the control cases. On blots, densitometric p-STAT3 levels in nuclear protein extracts significantly increased in the ALS group compared with the control group, although there was no significant difference in densitometric t-STAT3 levels in cytosolic protein extracts between the two groups. Additionally, there was no significant relationship between the nuclear p-STAT3 levels in the ALS cases and the clinical phenotypes, age at death, or disease duration. 〈 i 〉 Conclusion: 〈 /i 〉 The present results suggest that persistent activation and nuclear translocation but not upregulation of STAT3 occurs in ALS spinal cord microglia, which may regulate inflammatory activity.
Type of Medium:
Online Resource
ISSN:
1660-2854
,
1660-2862
Language:
English
Publisher:
S. Karger AG
Publication Date:
2009
detail.hit.zdb_id:
2126858-7
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