Skip to main content
. 2022 Mar 7;13:827146. doi: 10.3389/fimmu.2022.827146

Figure 2.

Figure 2

S1, through ACE2, upregulates adhesive molecules on HMEC-1 by impairing AMPK signalling. (A) Quantification and representative Western Blots of ACE2 protein expression in HMEC-1 exposed for 24h to medium alone (CTR) or S1 (10 nM). GAPDH was used as a sample loading control. (B–D) Quantification and representative images of ICAM-1 expression [(B), red], P-selectin expression [(C), red], and vWF deposition [(D), red] on HMEC-1 incubated with medium alone (CTR) or with S1 (10 nM) in the presence of anti-ACE2 Ab (2 μg/ml) or Irr Ab (2 μg/ml). (E) Quantification and representative Western Blots of AMPK activation, evaluated as the ratio between the expression of pAMPKThr172 and total AMPK in HMEC-1 exposed for 24h to medium alone (CTR) or S1 (10 nM). (F, G) Quantification of ICAM-1 expression (F) and vWF deposition (G) on HMEC-1 incubated with medium alone (CTR) or with S1 (10 nM) in the presence or absence of AMPK agonist AICAR (2 mM). All experiments were repeated at least 3 times. Data represent mean ± SEM and were analysed with unpaired t-test or Tukey’s multiple comparison test, as appropriate. **p-value<0.01, and ***p-value<0.001 vs CTR; °°°p-value<0.001 vs 10 nM S1; ###p-value<0.001 vs 10 nM S1+Irr. All slides were counterstained with DAPI (blue). Scale bar 20 μm for (B, C) and 50 μm for (D).