Fig. 4

Attenuation of TGFβ2-induced EndMT in HUVECs by MFNG deprivation. a Verification of the knockdown efficiency of three MFNG-targeted shRNAs with different interference sequences at the transcriptional level. b Western blot confirmed successful MFNG knockdown in HUVECs, with corresponding quantitative analysis. β-actin served as the loading control. c Representative images illustrating the endothelial morphological phenotype of HUVECs transduced with MFNG shRNA lentivirus. The morphology of HUVECs infected with equal doses of sh-NC and sh-MFNG differed in response to TGFβ2. MFNG knockdown in HUVECs blocked the morphological changes induced by TGFβ2. Scale bars = 25 µm. d Western blot displayed alterations in EndMT markers, along with corresponding quantitative analysis. β-actin was used as an internal control. e–h MFNG deprivation hindered TGFβ2-induced HUVEC migration. e, f Representative images of cell wound healing assays and quantification of the scratch repair rate. Scale bars = 250 µm. g, h The transwell migration assay was performed, and the relative number of migrated cells per high-power field was measured. Scale bars = 100 µm. All data reported are from three independently repeated biological experiments