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[Preprint]. 2025 Jun 4:2023.07.11.548558. Originally published 2023 Jul 11. [Version 3] doi: 10.1101/2023.07.11.548558

Figure 6. CREB signaling is impaired by Aβ40 oligomers and a TrkB agonist reduces Aβ40-mediated caspase 3 activation in human cardiomyocytes (AC16 cells).

Figure 6.

(A-C): Representative immunoblots (A-B) and densitometric quantitative analysis (C) of multiple independent experiments to evaluate CREB levels in nuclear extracts isolated from human cardiomyocytes (AC16) stimulated with human Aβ−40 oligomers for 15 minutes or 1h. LAMININ A/C levels were used as a nuclear loading control. (D-F): Representative immunoblots (D) and densitometric quantitative analysis (E-F) showing protein levels of BDNF in total protein lysates from human cardiomyocytes (AC16) stimulated with TrkB agonist LM22A-4 (100 nM) or TrkB antagonist ANA-12 (30 μM) for 16 h. GAPDH and ACTIN levels were used as loading controls. n=3–6. Data are presented as a mean±SEM. *P<0.05 and vs NT. Student t-tests have been performed between the groups. (G-I): Representative immunoblots (G) and densitometric quantitative analysis (H-I) of multiple independent experiments to evaluate Cleaved-Caspase 3 (Cl-Casp3) in AC16 cells stimulated with human Aβ−40 oligomers for 16 h. Before Aβ−40 oligomers treatment, cells were pretreated with either LM22A-4 (100 nM, top panel), or ANA-12 (30 μM, bottom panel) for 1 h. GAPDH levels were used as a loading control. n=6–12. One-way ANOVA with Tukey’s multiple comparisons post hoc test: *P<0.05 and vs NT. (NT= Not Treated).