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. 2015 Jun 15;112(27):8445–8450. doi: 10.1073/pnas.1504890112

Fig. 1.

Fig. 1.

PPARα deficiency results in impaired ADAM10 expression. (A–D) Quantitative PCR results of Adam10 (A), Adam17 (B), Bace1 (C), and Psen1 (D) mRNA expression in the hippocampus and cortex of 4-mo-old WT Ppara−/− and Pparb−/− animals or in WT neurons knocked down for PPARγ (PpargKD). Values are corrected for Gapdh and are expressed as percentage of WT. (E) Subcellular and detergent-soluble (1% CHAPS) expression of precursor (pA10) and mature (mA10) ADAM10 and COOH terminus cleaved ADAM10 (A10CTF) or precursor (pA17) and mature (mA17) ADAM17 in hippocampi from 4-mo-old WT animals. (F–J) Representative immunoblots (F) and quantification of pA10 (G), mA10 (H), A10CTF, pA17 (I), mA17 (J), and A17CTF membrane expression in the hippocampus and cortex of 4-mo-old WT, Ppara−/− and Pparb−/− animals or in 18DIV PpargKD neurons. (K and L) Representative immunoblots of detergent-soluble BACE1 (K), N-terminal and C-terminal presenilin-1 (PS1NT and PS1CT, respectively) (L) expression in the hippocampus of 4-mo-old Ppara WT (+/+) and null (−/−) animals. Values are corrected for α-tubulin, indicate the mean ± SEM relative to WT, and represent n = 3 or 4 for each genotype. *P < 0.05 and **P < 0.01 using one-way ANOVA. Ctx, cortex; Hpc, hippocampus; KD, knockdown; Neu, neurons; OD, relative optical density. ●, nonspecific band.