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. 2013 Aug 14;14(8):16719–16731. doi: 10.3390/ijms140816719

Figure 4.

Figure 4

TPC requires the presence of PN-1. (A) TPC was performed in slices from mice lacking PN-1. TPC before OGD significantly (p < 0.001, Kruskall Wallis followed by Dunn’s multiple comparisons) attenuated neuronal death in cultures from wild-type mice. TPC did not induce a significant protection (ns) in heterozygotes or knock-out mice, demonstrating that endogenous PN-1 is required for TPC. N represents the number of slices. (*** p < 0.001); (B) Given the identification of PN-1 as a target for TPC, slices from PN-1 KI mice were used to test whether the TPC-induced upregulation of PN-1 was influenced by the JNK inhibitor L-JNKI1, known to block the protective effect of TPC. β-galactosidase positive cells in the stratum radiatum were counted. TPC enhanced the expression of PN-1 (ANOVA p < 0.0001, Tukey-Cramer p < 0.001) while L-JNKI1 alone did not. The addition of L-JNKI1 after TPC significantly reduced the PN-1 upregulation (ANOVA p < 0.0001, Tukey-Cramer p < 0.001 compared to TPC alone). (*** p < 0.001).