Fig. 3

Knockdown of HSP110 inhibits hypoxia-induced autophagy and YAP/TAZ-TEAD4 activity in mice. Relative mRNA level (a) and protein level (b, c) of HSP110 pulmonary arteries in lung tissues in each group (N = 8). d Double immunofluorescence staining of α-SMA (green) and HSP110 (red) in pulmonary arteries (N = 8). White scale bars, 50 μm; Yellow scale bars, 25 μm. White arrows pointed to α-SMA and HSP110 double-positive cells. e Protein levels of LC3II, LC3I, Beclin1, ATG5, ATG7 and p62 in pulmonary arteries (N = 8). f–h Quantitative analysis of relative protein ratio of LC3-II/I and relative protein level of Beclin1, p62, ATG5 and ATG7 (N = 8). i Double immunofluorescence staining of α-SMA (green) and Beclin 1 (red) in pulmonary arteries (N = 8). Scale bars, 50 μm. j Protein levels of p-YAP, YAP, p-TAZ and TAZ in pulmonary arteries (N = 8). k Quantitative analysis of relative protein ratio of p-YAP/t-YAP and p-TAZ/t-TAZ (N = 8). l–n Nuclear protein levels of YAP, TAZ and TEAD4 and quantitative analysis of relative protein level of nuclear YAP, TAZ and TEAD4 (N = 8). o Double immunofluorescence staining of α-SMA (green) and YAP (red) in pulmonary arteries (N = 8). White scale bars, 50 μm; Yellow scale bars, 25 μm. White arrows pointed to α-SMA and YAP double-positive cells. Data are means ± SD from 8 mice per group. *p < 0.05 compared to the normoxia group. ^#p < 0.05 compared to the hypoxia-shNC group