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. Author manuscript; available in PMC: 2024 Sep 10.
Published in final edited form as: Circ Res. 2020 Jun 12;127(6):707–723. doi: 10.1161/CIRCRESAHA.119.316071

Figure 7. B55α induces cell protection against ROS and cell stress partially in a PHD dependent manner.

Figure 7

(A) WBs showing that the upregulation of B55α under dense conditions can be partially inhibited with the ROS scavenger MnTBAP

(B) ROS sensitivity assay analyzing the differential effects of H2O2-induced ROS on sparse, confluent and dense HUVECs.

(C) Analysis of ROS sensitivity in qVD treated HUVECs showing the differential response of B55α-KD HUVECs to H2O2 induced ROS-stress under dense conditions.

(D,E) WB analysis of different proteins indicating increased cell stress (such as p-eIF2α and p21), proteins involved in counteracting cell stress (HIF1α, HIF2α, p-AKT) and the apoptosis marker cleaved Caspase3 in B55α-KD and DMOG treated HUVECs.

(F-M) qPCR-based expression analysis of B55α (F,G), genes counteracting ROS (Catalase (H), SOD1 (I), SOD2 (J), GLRX (K)) and EC maturation markers such as total Vegfr1 (L), and VEcadherin (M).

(N-P) Staining of Phalloidin and Hoechst in DMOG treated B55α-KD and control HUVECs (Scale bar: 100µm) (N) and quantification of the increased resistance to H2O2 (O) and cell survival (P).

(Q,R) Representative images of sponges stained for CD31+ blood vessels (Scale bar: 300µm)

(Q) and quantification thereof (n = 6 per group) (R).

P values are *p<0,05; **p<0,001; ***p<0,001; ****p<0,0001.

Graphs show standard error of the mean (SEM).