Fig. 7: FNDC4 elevates HIF1α protein level through suppressing its proteasomal degradation. | Nature Communications

Fig. 7: FNDC4 elevates HIF1α protein level through suppressing its proteasomal degradation.

From: FNDC4 alleviates cardiac ischemia/reperfusion injury through facilitating HIF1α-dependent cardiomyocyte survival and angiogenesis in male mice

Fig. 7

a, b NRCMs with FNDC4 overexpression or knockdown were treated with cycloheximide (CHX) to inhibit protein synthesis, and western blot was performed to analyze HIF1α protein levels at the indicated time points (n = 6 independent experiments). c NRCMs with FNDC4 knockdown were treated with proteasomal inhibitors (BZM and CFZ) or lysosomal inhibitors (E-64d and leupeptin), and western blot was performed to measure HIF1α protein level (n = 6 independent experiments). d The top 10 downregulated GO terms of the transcriptome analysis (n = 3). e The expressions of proteasome-related genes were presented using a heatmap (n = 3). f Heart samples were collected from von Hippel-Lindau protein (Vhl) cKO mice with or without FNDC4 knockdown 24 h after I/R surgery, and then exposed to Evans blue and TTC double staining (n = 6). g Cardiac function of Vhl cKO mice with or without FNDC4 knockdown was analyzed by transthoracic echocardiography at the indicated time points (n = 6). Data were presented as the mean ± S.D., and analyzed using repeated measures ANOVA. For the analysis in (c), one-way ANOVA followed by Tukey post hoc test was used. For the analysis in (f), an unpaired two-tailed Student′s t-test was used. *P < 0.0001. Source data are provided as a Source Data file.

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