Data for: Seipin deletion in mice enhances phosphorylation and aggregation of tau protein through reduced neuronal PPARγ and insulin resistance
Description
We attached the independent replicates of Western blot analyses in the supplementary section that were used in various quantifications. The regions of line rectangles in these blots/gels, as representative images, were used in Figures of the main Text. In the Fig. 1e: the levels of hippocampal NF-H protein in seipin-sKO mice (sKO) and seipin-nKO mice (nKO) were lower than those of WT mice. In the Fig. 2a: the levels of tau protein in hippocampus of seipin-sKO mice, seipin-nKO mice and seipin-aKO mice (aKO) were not altered. In the Fig. 2b: the levels of oligomer tau protein were increased in seipin-sKO mice and seipin-nKO mice. In the Fig. 2c: the levels of hippocampal tau phosphorylation at Thr212/Ser214 and Ser202/Thr205 were increased in seipin-sKO mice and seipin-nKO mic. In the Fig. 3a: the levels of PPARγ protein were decreased in hippocampus of seipin-sKO mice and seipin-nKO mice. In the Fig. 3b: the administration of PPARγ agonist rosiglitazone (rosi) for 7 days could correct the increased tau phosphorylation at Thr212/Ser214 and Ser202/Thr205 in seipin-sKO mice and seipin-nKO mice. In the Fig. 4a: seipin-sKO mice and seipin-nKO mice showed an increase in the GSK3β phosphorylation at Tyr21 and a decrease at Ser9, which were corrected by rosi. In the Fig. 4b: the treatment with AR-A014418 (AR) corrected the increased tau phosphorylation at Thr212/Ser214 and Ser202/Thr205 in seipin-nKO mice. In the Fig. 5a&5b: the phosphorylation of Akt and mTOR was elevated in seipin-sKO mice and seipin-nKO mice, which were corrected by rosi. In the Fig. 5c&5d: seipin-sKO mice and seipin-nKO mice showed a decrease in the ratio of LC3II/I and an elevation of p62 protein, which was rescued by the PI3K inhibitor LY294002 (LY) and mTOR inhibitor rapamycin (Rap), but not AR. In the Fig. 5e&5f: the administration of LY and Rap reduced the levels of oligomer tau protein and tau phosphorylation at Thr212/Ser214 and Ser202/Thr205 in seipin-nKO mice. In the Fig. 6c: the increased phosphorylation of JNK in seipin-sKO mice were corrected by treatment with rosi for 30 days. In the Fig. 6d: the P38 phosphorylation in seipin-sKO mice was not altered. In the Fig. 6e: the increased phosphorylation of tau at Ser396 in seipin-sKO mice was prevented by treatment with rosi for 30 days and the JNK inhibitor SP600125 (SP).