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. 2024 Nov 22;13(23):e036969. doi: 10.1161/JAHA.124.036969

Figure 4. Knockdown of VCAN inhibited hypoxia‐induced EndMT in vitro.

Figure 4

A, The workflow diagram of the in vitro experiment. (B–D) Representative images and densitometric quantification of migration and invasion assay of HPAECs (n=3). ×100, scale bar: 100 μm. ***P<0.001. (E) Co‐immunostaining of VCAN (red) with vWF(green) was performed in HPAECs (n=3). ×400, scale bar: 25 μm. (F) Co‐immunostaining of CD31 (red) with α‐SMA (green) was performed in HPAECs (n=3). ×400, scale bar: 25 μm. (G) Densitometric fluorescence intensity of VCAN, CD31, and α‐SMA in (4F and 4G) (n=3). **P<0.01, ***P<0.001. (H and I) The protein levels and densitometric quantification of VCAN, CD31,VE‐cadherin, vimentin, and α‐SMA were determined by Western blot analysis after different treatment (n=3). *P<0.05, ***P<0.001. ANOVA with the Tukey test was performed for comparison between 4 groups. CD31 indicates platelet endothelial cell adhesion molecule‐1; EndMT, endothelial‐to‐mesenchymal transition; H&E, hematoxylin–eosin; HPAECs, human pulmonary artery endothelial cells; siRNA, small interfering RNA; VCAN, versican; VE‐cadherin, vascular endothelial cadherin; vWF, von Willebrand factor; and α‐SMA, α‐smooth muscle Actin.