Fig. 2: Ang II-induced dysregulation of the TA proteome was greater in ANXA1-/- than WT mice, and this effect was greater in females than males. | Communications Biology

Fig. 2: Ang II-induced dysregulation of the TA proteome was greater in ANXA1-/- than WT mice, and this effect was greater in females than males.

From: Annexin-A1 deficiency uncovers female-specific pathways in blood pressure control and cardiovascular remodeling in mice

Fig. 2

Upregulated (orange) and downregulated (green) cellular components in TA (A). Venn diagram displaying Ang II-regulated change in proteins identified and their abundance in TA of WT and ANXA1-/- mice of both sexes (B, C). Volcano plot comparing structural (red), calcium regulatory (orange), inflammatory (green), oxidative stress (purple), and mitochondrial (blue) proteins in TA of hypertensive WT and ANXA1-/- mice of both sexes (B, C). Heat map comparing structural (red), calcium regulatory (orange), inflammatory (green), oxidative stress (purple), and mitochondrial (blue) proteins in TA of hypertensive WT (n = 4–5) and ANXA1-/- mice (n = 5) and normotensive WT (n = 4–5) of both sexes (D, E). Heatmap compared the expression of differential proteins in WT mice-infused with Sal or Ang II (light purple), WT and ANXA1-/-mice-infused with Ang II (dark purple), and WT and ANXA1-/- mice-infused with Sal or Ang II (darkest purple) in TA of both sexes (D, E). Fold change of proteins with P < 0.05 (calculated with Student’s t test) was considered statistically significant. Ang II: angiotensin II, ANXA1-/-: annexin-A1-deficient, GO: gene ontology annotation, Sal: saline, TA: thoracic aorta, WT: wild-type.

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