Periostin Induces the Proliferation of Pulmonary Artery Smooth Muscle Cell Through ERK1/2 Signaling Pathway
Objective To explore the role and mechanism of periostin(POSTN)in the proliferation of pulmonary artery smooth muscle cell(PASMC)in hypoxia-induced pulmonary hypertension(HPH).Methods The primary PASMC from male rats were ex-posed to hypoxic environment to simulate HPH.The cells were divided into normoxia group,hypoxia group,hypoxia+control adenovirus transfected group(hypoxia+Ad-shNC group),hypoxia+POSTN silenced adenovirus transfected group(hypoxia+Ad-shPOSTN group),POSTN group,POSTN+U0126 group.α-smooth muscle actin(α-SMA)was used to evaluate the purity of PASMC,CCK-8 assay was performed to detect cell viability,and Western blot was utilized to detect the protein expression level of POSTN,proliferating cell nuclear antigen(PCNA),bone morphogenetic protein type Ⅱ receptor(BMPR2),phosphorylated extracellular signal-regulated ki-nase 1/2(p-ERK1/2),and extracellular signal-regulated kinase 1/2(ERK1/2)in PASMC.Results Compared with the normoxia group,hypoxia promoted the proliferation of PASMC and the expression level of POSTN protein,while inhibited the expression level of BMPR2 protein.Down-regulation of POSTN expression could inhibit hypoxia-induced proliferation of PASMC and restore BMPR2 pro-tein expression level.In addition,POSTN significantly increased the protein expression ratio of p-ERK1/2 or ERK1/2,and the prolifer-ation of PASMC,which could be blocked by U0126.Conclusion In the pathological mechanism of HPH,POSTN promotes the prolifera-tion of PASMC,and its potential mechanism may be related to the regulation of BMPR2 expression and activation of ERK1/2 signaling pathway.
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