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. Author manuscript; available in PMC: 2009 Sep 1.

Published in final edited form as: Exp Neurol. 2008 May 29;213(1):114–121. doi: 10.1016/j.expneurol.2008.05.014

Evidence that TLR4 mediates activation of JNK and caspase-3 in response to Aβ and HNE in cortical neurons. Immunoblot analysis of phospho-JNK (46 kDa), total JNK (46 kDa) and cleaved caspase-3 (19 kDa) in cell lysates of neurons in cortical cultures established from either wild-type (WT) or TLR4 deficient (TLR4mu) mice. The neurons were left untreated or were exposed to 5 μM Aβ1-42 (panel A) or 5 μM HNE (panel C) for the indicated time points. Results of densitometric analysis of phospho-JNK and cleaved caspase-3 protein levels in WT compared with TLR4 mutant cells from Aβ treated (panel B) and HNE treated (panel D) samples at 24 hours. Analyses were performed on pooled samples from at least 3 separate cultures that had been established from 10-14 embryos in each group.

Evidence that TLR4 mediates activation of JNK and caspase-3 in response to Aβ and HNE in cortical neurons. Immunoblot analysis of phospho-JNK (46 kDa), total JNK (46 kDa) and cleaved caspase-3 (19 kDa) in cell lysates of neurons in cortical cultures established from either wild-type (WT) or TLR4 deficient (TLR4mu) mice. The neurons were left untreated or were exposed to 5 μM Aβ1-42 (panel A) or 5 μM HNE (panel C) for the indicated time points. Results of densitometric analysis of phospho-JNK and cleaved caspase-3 protein levels in WT compared with TLR4 mutant cells from Aβ treated (panel B) and HNE treated (panel D) samples at 24 hours. Analyses were performed on pooled samples from at least 3 separate cultures that had been established from 10-14 embryos in each group.