NF-B activity is inversely correlated to RNF11 expression in Parkinson’s disease

• Type of Material: Article
• Authors: Elaine Pranski, Emory University; Carson .D. Van Sanford, Emory University; Nirjari Dalal, Emory University; Adam L. Orr, Emory University; Dipan Karmali, Emory University; Deborah S Cooper, Emory University; Marla Gearing, Emory University; James J Lah, Emory University; Allan I Levey, Emory University; Ranjita Betarbet, Emory University
• Language: English
• Date: 2013-06-28
• Publisher: Elsevier: 12 months
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2013 Elsevier Ireland Ltd. All rights reserved.
• License: Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1016/j.neulet.2013.04.056
• Title of Journal or Parent Work: Neuroscience Letters
• ISSN: 0304-3940
• Volume: 547
• Start Page: 16
• End Page: 20
• Grant/Funding Information: This research project was supported in part by the microscopy cores of the Emory Neuroscience NINDS Core Facilities grant, P30NS055077.; We thank the National Institutes of Health through the Alzheimer’s Disease Research Center grant (AG025688), NIEHS ES015777 (RSB), NIEHS ES012870 (ELP), and NINDS NS007480 (ELP).
• Keywords: phospho-p65; immunofluorescence; cingulate cortex; substantia nigra
• Research Categories: Health Sciences, Pathology; Health Sciences, Mental Health; Biology, Neuroscience

Abstract

RING finger protein 11 (RNF11), a negative regulator of NF-κB signaling pathway, colocalizes with α-synuclein and is sequestered in Lewy bodies in Parkinson’s disease (PD). Since persistent NF-κB activation is reported in PD, in this report we investigated if RNF11 expression level is correlated to activated NF-κB in PD. We examined RNF11 expression levels in correlation to phospho-p65, a marker for activated NF-κB, in control and PD brain tissue from cerebral cortex. In addition we performed double immunofluorescence labeling experiments to confirm this correlation. Our investigations demonstrated that the neuronal RNF11 expression was down-regulated in PD and was usually associated with increased expression of phospho-p65. Double labeling confirmed that loss of neuronal RNF11 was linked to increased phospho-p65 expression, suggesting that persistent presence of NF-κB activation could be due to decreased levels of its negative regulator. Our data exemplifies the relevance of RNF11 and persistent NF-κB activation in PD.