Effect of annexin A2 on hepatopulmonary syndrome rat serum-induced proliferation of pulmonary arterial smooth muscle cells

Hepatopulmonary syndrome (HPS) is characterizes by an arterial oxygenation defect induced by intrapulmonary vasodilation that increase morbidity and mortality. However, the underlying mechanisms on HPS-associated pulmonary vascular remodeling remains undefined. In this study, we found that HPS rat serum, drawn from common bile duct ligation (CBDL) rats, mediated the overexpression of ANXA2 and the proliferation of PASMCs. And small interfering RNA (siRNA) that target rat ANXA2 led to significant downregulation of ANXA2, which resulted in the decreased proliferation of PASMCs. Subsequently, we further examined the role of ANXA2 siRNA in the regulation of pro-proliferative signaling such as that mediated by ERK1/2 and NF-κB, and found the attenuation of HPS-associated activation of the signaling pathway. Thus, the fact highlighted the crucial role of ANXA2 in HPS-associated PASMC proliferation, and suggested a potential therapeutic effect on HPS-associated pulmonary vascular remodeling.

► Hepatopulmonary syndrome (HPS) rat serum stimulated the proliferation of PASMCs.
► The expression of ANXA2 was up-regulated under the HPS rat serum condition.
► ANXA2 siRNA reversed positive effect of HPS rat serum on PASMC proliferation.
► ANXA2 siRNA attenuated the activation of ERK1/2 and NF-κB.
► ANXA2 plays an important role in HPS rat serum-induced PASMC proliferation.