Skip to main content
Fig. 3 | Molecular Medicine

Fig. 3

From: ADSCs enhance VEGFR3-mediated lymphangiogenesis via METTL3-mediated VEGF-C m6A modification to improve wound healing of diabetic foot ulcers

Fig. 3

ADSCs regulate VEGF-C expression via the METTL3/IGF2BP2-m6A pathway. sh-METTL3 and pcDNA-METTL3 plasmids were transfected into ADSCs for METTL3 knockdown and overexpression, respectively. sh-NC served as the negative control for sh-METTL3, and the pcDNA-empty vector served as the negative control for pcDNA-METTL3 plasmids. A MeRIP-qPCR was performed to assess the m6A levels of VEGF-C mRNA. B Western blotting was conducted to measure the levels of VEGF-C proteins. C An ELISA was carried out to assess the levels of VEGF-C in the supernatant of ADSCs. D, E RNA pulldown and RIP assays were performed to evaluate the interaction between VEGF-C and IGF2BP2. Immunoblotting of IGF2BP2 after RNA pulldown assay with cell lysate (Ly) and full-length biotinylated VEGF-C (FL); NC indicates the beads. sh-IGF2BP2 plasmids were transfected into ADSCs for IGF2BP2 knockdown, and sh-NC served as the negative control for sh-IGF2BP2 plasmids. F RT-qPCR was performed to assess the levels of IGF2BP2. G Western blotting was conducted to measure the protein levels of IGF2BP2 and VEGF-C. Data represent the mean of three independent experiments. Error bars represent SD. *P < 0.05, **P < 0.01 or ***P < 0.001

Back to article page