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. 2024 Jan 13;15(1):45. doi: 10.1038/s41419-023-06416-5

Fig. 5. IFITM3 regulates GSC-mediated angiogenesis process in a bFGF-dependent manner.

Fig. 5

A GSC#1-shScr or GSC#1-shIFITM3 were cultivated for 24 h, of which culture media were harvested for cytokine detection using angiogenesis antibody array. B GSC#2 cells were fractionated into IFITM3+ or IFITM3-groups, and angiogenic cytokines were measured. C Bar charts show markedly altered cytokines of (A) and (B). D Secreted bFGF levels of GSC#1–5 were measured using Elisa assay. E Representative immunofluorescent images with bFGF (red) staining of GSC#1-shScr and GSC#1-shIFITM3. F-actin (green) is stained with phalloidin. Nuclei are counterstained with Dapi (blue). Scale bar = 50 μm. F Angiogenic abilities of fractionated IFITM3 and IFITM3+ GSCs are measured, with the latter cells treated with manipulated bFGF downregulation. G Intracranial xenograft models are constructed with GSC#1-shScr and GSC#1-shIFITM3. Tumor sizes are monitored by in vivo imaging. H Representative immunofluorescence images staining for IFITM3 (green) and bFGF (red) and in GSC#1-shScr or GSC#1-shIFITM3 xenografts. I Representative immunofluorescence images staining for IFITM3 (green), bFGF (red), and CD34 (purple) in human GBM samples. J Schematic illustration of GSCs-mediated glioma angiogenesis through IFITM3-JAK/STAT-bFGF signaling pathway. Results are represented as Mean ± SD of biologically triplicate assays. *p < 0.05, **p < 0.01, ***p < 0.001. ns not significant.