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. 2020 Jul 23;10(20):9280–9302. doi: 10.7150/thno.46566

Figure 7.

Figure 7

The activity of TFE3 after SCI is regulated by AMPK-mTOR and AMPK-SKP2-CARM1 signaling pathways. (A) Western blot analysis of AMPK-mTOR signal pathway in the cytoplasm in spinal cords from the control mice, SCI mice, and SCI mice treated with DMSO or Compound C, at Day3. (B) Densitometric analysis of the AMPK, p-AMPK, p-mTOR and p-4EBP1 data from (A), normalized to the loading control GAPDH. (C) Western blotting of TFE3 nuclear translocation at the lesion for each group. (D) Corresponding densitometric analysis of the TFE3 bands in (C) normalized to the loading control H3. (E) Western blots of the AMPK-SKP2-CARM1 signaling pathway in the nucleus of the indicated groups at Day3 after SCI. (F) Densitometric analysis of AMPK, p-AMPK, p-FOXO3a, SKP2 and CARM1 bands from (E) normalized to control H3. (G) Nuclear CARM1-TFE3 complex was detected by IP in indicated groups at Day3 after SCI. (H) Densitometric analysis of TFE3 and CARM1 data from (G) normalized to loading control H3. (I) Western blot analysis of LC3, SQSTM1/p62 and UB in the spinal cord lesion of each group at Day3 after SCI. (J) Densitometric analysis of band data from (I) normalized to the loading control GAPDH. (K) Western blotting of LC3II in the indicated mice spinal cord slides cultured in the presence or absence of CQ at Day3. (L) Densitometric analysis of LC3II from (K) normalized to the loading control GAPDH. n=6, ns stands for not significant, *P<0.05, **P<0.01.