Extended Data Fig. 4: TGF-β activation in HF. | Nature Neuroscience

Extended Data Fig. 4: TGF-β activation in HF.

From: Heart failure-induced cognitive dysfunction is mediated by intracellular Ca2+ leak through ryanodine receptor type 2

Extended Data Fig. 4: TGF-β activation in HF.The alt text for this image may have been generated using AI.

a) Immunoblots showing expressing levels of TGF-β, phosphorylated SMAD3, total SMAD3, and NOX2 binding to RyR2 in the hippocampi of controls (n = 4) and HF patients (n = 9). b) Bar graphs depicting the ratio of TGF-β expression normalized to GAPDH, phosphorylated SMAD3 to total SMAD3 and NOX2 binding to RyR2 (IP RyR2). The same quantity of proteins were loaded on two separate gels and blotted separately for SMAD3 and pSMAD3. Individual values are shown with mean ± SEM (t-test * p < 0.05, Controls vs. HF patients). c) Immunoblots showing expressing levels of TGF-β, phosphorylated SMAD3, total SMAD3, and NOX2 binding to RyR2 in the hippocampi of SHAM, MI, MI + ARM036, MI + S107, MI+ propranolol and MI + SD-208 mice (n = 6, 6, 6, 6, 4 and 4 respectively). d) Bar graphs depicting the ratio of TGF-β expression normalized to GAPDH, phosphorylated SMAD3 to total SMAD3 and NOX2 binding to RyR2 (IP RyR2). The same quantity of proteins were loaded on two separate gels and blotted separately for SMAD3 and pSMAD3. Individual values are shown with mean ± SEM. One-way ANOVA and Tukey’s test post-hoc correction for multiple comparisons shows * p < 0.05, SHAM vs. MI, MI + ARM036 or MI + S107; #p < 0.05, MI vs. MI + S107, MI+ propranolol or MI + SD-208. All statistical tests were two-sided. Data are derived from biologically independent samples.

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