Skip to main content
. 2017 May 22;40(1):65–74. doi: 10.3892/ijmm.2017.2998

Figure 4.

Figure 4

Knockdown of runt-related transcription factor 3 (RUNX3) attenuates endothelial-mesenchymal transition (EndMT) of human cardiac microvascular endothelial cells (HCMECs). (A) RT-PCR data showing the mRNA expression levels of the endothelial markers (CD31 and VE-cadherin) and mesenchymal markers [fibroblast-specific protein (FSP)-1 and α-smooth muscle actin (α-SMA)] in the HCMECs. Results were normalized to reference gene β-actin (n=7, *P<0.05 vs. control group; #P<0.05 vs. hypoxia group; ▲P<0.05 vs. RUNX3i group). (B) Relative protein expression of CD31, VE-cadherin, FSP-1 and α-SMA to GAPDH in the HCMECs from each group (n=7, *P<0.05 vs. control group; #P<0.05 vs. hypoxia group; ▲P<0.05 vs. RUNX3i group). (C) Double immunofluorescence staining with antibodies to CD31 (red) and α-SMA (green). Nuclei were counterstained with DAPI (blue). The expression of CD31 was downregulated and α-SMA upregulated in the hypoxia group compared with the control group. Scale bars, 50 μm. (D) Double immunofluorescence staining with antibodies to CD31 (red) and α-SMA (blue). The expression of CD31 was upregulated and α-SMA was downregulated in the RUNX3i group compared with the green fluoresent protein (GFP) group. Scale bars, 50 μm.