Fig 1: CHI3L1 prompted angiogenesis of HUVECs in vitro (magnification 100×). Representative images of angiogenesis of HUVECs. IL-13Ra2 shRNA, MEK (PD98059) inhibitor, and PI3K (LY294002) inhibitor inhibited the angiogenesis capacity stimulated with CHI3L1 (A). The qualification of branch points number was calculated (B). Data were presented as mean ± SD (n = 3 per group). *p < 0.05, **p < 0.01, and ***p < 0.001.
Fig 2: Western blot analysis of ERK and AKT in HUVECs. CHI3L1 prompted the phospho-ERK and phospho-AKT expression of HUVECs, and IL-13Ra2 shRNA decreased expression of phospho-ERK and phospho-AKT (A). The expression ratio of phosphorylated ERK and AKT to total ERK and AKT was determined by densitometric analysis (B,C). Data were presented as mean ± SD (n = 3 per group), **p < 0.01 and ***p < 0.001.
Fig 3: The migration of HUVECs was measured via transwell assay (magnification 200×). The effects of CHI3L1 on HUVECs migration were tested in the presence or absence of IL-13Ra2 shRNA, MEK (PD98059) inhibitor, and PI3K (LY294002) inhibitor (A). The number of migration cells was calculated (B). Data were presented as mean ± SD (n = 3 per group). *p < 0.05, **p < 0.01, and ***p < 0.001.
Fig 4: Interference effect of Ad.IL-13Ra2 shRNA and optimal concentration of CHI3L1 for proliferation. Interference effect of Ad.IL-13Ra2 shRNA on membrane protein of IL-13Ra2 in human umbilical vein endothelial cells (HUVECs) measured by Western blotting (A,B). The CCK-8 assay was performed to investigate the proliferation of HUVECs with different concentrations of CHI3L1 at 24 and 48 h, respectively (C). The inhibition effect of Ad.IL-13Ra2 shRNA on the expression of IL-13Ra2 in the aorta was analyzed by immunohistochemistry (D,E). Data were presented as mean ± SD (n = 3 per group). **p < 0.01 and ***p < 0.001.
Supplier Page from Abcam for Recombinant Human YKL-40/CHI3L1 protein