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. 2019 Oct 13;17(2):240–253. doi: 10.1080/15476286.2019.1676114

Figure 2.

Figure 2.

Involvement of HECTD1 in cell viability changes induced by I/R in HUVECs. (A) Representative western blot and densitometric analyses showing the efficacy of HECTD1 CRISPR ACT in increasing the level of the HECTD1 protein in HUVECs. *P < 0.05 vs. the control group, n = 5. (B) CCK-8 assay showing that HECTD1 ACT attenuated the I/R-induced decrease in HUVEC viability. **P < 0.01 vs. the control group, **P < 0.001 vs. the control group; ##P < 0.01 vs. the I/R group, n = 5. (C) Representative images of Hoechst 33342 staining of HUVECs after I/R. (D) Hoechst 33342 staining demonstrating that apoptosis induced by I/R was attenuated by upregulation of HECTD1 expression with ACT in HUVECs; n = 5; *P < 0.05 vs. the control group, ***P < 0.001 vs. the control group; ###P < 0.001 vs. the I/R group. (E) Representative western blot showing the effect of specific upregulation of HECTD1 expression with ACT on I/R-induced apoptosis marker expression. (F) Densitometric analyses of five separate experiments suggesting that the I/R-induced changes in the Bax/Bcl2l1 ratio are attenuated by HECTD1 ACT. *P < 0.05 vs. the control group; #P < 0.05 vs. the I/R group. (G) Representative images of the BrdU labelling assay in HUVECs after I/R. (H) BrdU labelling assay results demonstrating that the decrease in proliferation induced by I/R was attenuated by HECTD1 ACT; n = 5; **P < 0.01 vs. the control group; ##P < 0.01 vs. the I/R group.