HepG2.2.15-derived exosomes facilitate the activation and fibrosis of hepatic stellate cells

Figure 3 The role of HepG2. 2.15-derived exosomes in LX2 proliferation and fibrosis. A: HepG2.2.15-derived exosomes (colored in yellow), highly expressing α-smooth muscle actin (SMA) (shown in green), are illustrated as being internalized by LX2 cells. The cells showcase a spindled shape and notable pseudopodia with some exosomes penetrating the cell nucleus (depicted in blue). The scale bar signifies 100 μm for reference; B: The HepG2-derived exosomes (yellow) exhibit lower expression levels of α-SMA (green) within the cytoplasm of the internalizing LX2 cells. Again, several exosomes can be observed within the cell nuclei (shown in blue). The same scale is applied; C: The expression of fibrosis marker proteins, namely α-SMA, COL1A1 type, MMP2, TIMP-1, and CTGF, within LX2 cells are verified through a Western blotting assay; D: Quantitative analysis of Western blotting was done on the intensity of fibrosis marker protein bands; E and F: The 5-ethynyl-2′-deoxyuracil cell proliferation experiment presents that the exosomes secreted by hepatitis B virus-infected hepatocytes have the capabilities of promoting LX2 cell proliferation. A 100 μm scale bar is used (Error bars represent the mean ± SD; ^aP < 0.05; ^cP < 0.001; ^dP < 0.0001). EDU: 5-ethynyl-2′-deoxyuracil; α-SMA: α-smooth muscle actin.