Fig. 4: AGGF1 promoted angiogenesis by upregulating proliferation-related indicators.

a Heat maps from proteomic array analysis with ranked enriched genes between control and AGGF1-silenced HRMECs treated with HG (fold-change >1.2 or <0.83, p  <  0.05). High and low expression are denoted by red and navy, respectively (n  =  3 independent cultures). b, c GO terms and KEGG pathway analysis of the differentially expressed genes between control and AGGF1-silenced HRMECs treated with normal glucose and HG. Statistical analysis was performed using Fisher exact test. d, e Western blot analysis and quantification of AGGF1, CyclinA2, CyclinD1 and CDK1 protein levels in control and AGGF1-silenced HRMECs treated with HG (n  =  6 independent cultures). f Cell proliferation was performed by EdU staining of control and AGGF1-silenced HRMECs treated with HG (n  =  3 independent cultures). g, h Representative images and quantification of control and AGGF1-silenced HRMECs treated with HG in wound healing assay at 0 and 24 h (n  =  3 independent cultures). i Representative images of angiogenesis in control and AGGF1-silenced HRMECs treated with HG, measured using in vitro tube formation assays (n  =  3 independent cultures). Error bars represent mean ± SEM. 2-tailed unpaired Student’s t test (a, e, h). Scale bars: 100 μm (f, i), 1000 μm (g). HG high glucose (33.3 mmol/L). Source data are provided as a Source Data file.