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ASN NEURO (2009) 1(2):art:e00010.doi:10.1042/AN20090009

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Inflammatory cytokines IL-1β and TNF-α regulate p75^NTR expression in CNS neurons and astrocytes by distinct cell-type-specific signalling mechanisms

Soyoung Choi and Wilma J Friedman¹

Department of Biological Sciences, Rutgers University, Newark, NJ 07102, U.S.A.

¹To whom correspondence should be addressed (email wilmaf@andromeda.rutgers.edu).

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SUPPLEMENTARY DATA

Figure S1 Confirmation that inhibitors of p38 MAPK and NF-κB inhibit their respective pathways

Treatment of hippocampal astrocytes with (A) IL-1β or (B) TNF-α in the absence or presence of the p38 MAPK inhibitor showed that SB203580 inhibited p38 MAPK phosphorylation induced by either ligand. (C) To confirm the inhibitory effect of SN-50 on NF-κB nuclear translocation, astrocytes were pretreated with vehicle or with 10 μM SN-50 for 30 min and then treated with IL-1β or TNF-α for 30 min. Cells were fixed and stained for p65, and nuclei were labelled with Hoechst stain. Nuclear staining of p65 was observed in IL-1β- or TNF-α-treated astrocytes without SN-50 (indicated by arrows; note the pink colour of the nuclei), and nuclear translocation of p65 was blocked by SN-50 (bottom panels).

Figure S2 Hippocampal neurons were treated with or without biotin

Cells were processed as indicated in Figure 6 of the main paper, lysates were precipitated with streptavidin and analysed by Western blot for p75^NTR levels. In the absence of biotin, no p75^NTR was detected.

Received 2 February 2009/7 April 2009; accepted 22 April 2009

Published as ASN NEURO Immediate Publication 22 April 2009, doi:10.1042/AN20090009

©2009 The Author(s) This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Licence (http://creativecommons.org/licenses/by-nc/2.5/) which permits unrestricted non-commercial use, distribution and reproduction in any medium, provided the original work is properly cited.