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Alban Gaultier, Sanja Arandjelovic, Xiaoqing Li, Julie Janes, Nikola Dragojlovic, George P. Zhou, Jenny Dolkas, Robert R. Myers, Steven L. Gonias, W. Marie Campana
Published in Volume 118, Issue 1
J Clin Invest. 2008; 118(1):161–172 doi:10.1172/JCI32371
Abstract | Full text | PDF
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Figure 8
sLRP-α antagonizes TNF-α–initiated cell signaling in astrocytes and microglia.

(A) Astrocyte cultures are immunopositive for GFAP (anti-GFAP, red). Cell nuclei were stained with DAPI (blue). (B) Astrocytes were cultured in serum-free medium for 1 h to reduce the basal level of activation of ERK/MAPK. The cells were then treated with TNF-α (1 nM) or vehicle for 10 min. Cell extracts were subjected to immunoblot analysis to detect P-ERK1/2 and T-ERK1/2. Some cells were pretreated with vehicle or sLRP-α (50 nM) for 10 min prior to adding TNF-α (1.0 nM) for 10 min. The blot is representative of 2 independent studies. (C) Microglial cell cultures were immunopositive for the complement receptor CR3, as determined with antibody OX-42 (green). Cell nuclei were stained with DAPI (blue). (D) Microglia were pretreated with vehicle of sLRP-α for 10 min and then treated with TNF-α (1.0 nM). Extracts were subjected to immunoblot analysis to detect P-p38. β-Actin was used as a loading control.