Fig. 1

CIH induced pulmonary hypertension in mice and p-STAT6 was upregulated in CIH-treated mice. Mice were exposed to Nor or CIH conditions for 6 weeks. PVSP (A), RV/(LV + S) (B) and pulmonary blood flow velocity (C) were measured. (D) The respective H&E and Masson stain of pulmonary arterioles in Nor and CIH groups were presented. (E) The percentage wall thickness of pulmonary arterioles was defined as the area occupied by the vessel wall divided by the total cross-sectional area of the arteriole. (F-G) Western blot analysis of p-STAT6, total-STAT6 and α‐SMA protein in the mice lungs from the two groups. (H) Immunohistochemistry analysis of p-STAT6 expression in mice lungs from the two groups. (I) The relative fluorescence density of p-STAT6 were measured. Data are presented as the mean ± SD (n = 6 per group). No significant difference is indicated by ns. Significant differences are presented as *(p < 0.05), **(p < 0.01), ***(p < 0.001) and determined by Student’s t‐test unless specified. Nor: normoxia; CIH: chronic intermittent hypoxia; RVSP: Right ventricular systolic pressure; H&E: hematoxylin and eosin