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Hypoxia-inducible factor 1a induces phenotype switch of human aortic vascular smooth muscle cell through PI3K/AKT/AEG-1 signaling

Kai Liu, Changcun Fang, Yuwen Shen, Zhengqin Liu, Min Zhang, Bingbing Ma and Xinyan Pang _

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Oncotarget. 2017; 8:33343-33352. https://doi.org/10.18632/oncotarget.16448

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Kai Liu1, Changcun Fang1, Yuwen Shen1, Zhengqin Liu1, Min Zhang1, Bingbing Ma1 and Xinyan Pang1

1Department of Cardiovascular Surgery, Qilu Hospital of Shandong University, Jinan 250012, Shandong, China

Correspondence to:

Xinyan Pang, email: [email protected]

Keywords: HIF-1a, HASMC, PI3K/AKT/AEG-1

Received: December 28, 2016    Accepted: March 09, 2017    Published: March 22, 2017


To date, hypoxia-inducible factor 1a (HIF-1a) and astrocyte elevated gene-1 (AEG-1) have been involved in the proliferation, migration and morphological changes of vascular smooth muscle cells. However, the potential relationship of HIF-1a-AEG-1 pathway in human aortic smooth muscle cell (HASMC) has not been reported. In the present study, in-vitro assays were utilized to explore the potential impact of HIF-1a-AEG-1 signaling on HASMC phenotype. Here, we found that HIF-1a expression was up-regulated in the media of thoracic aortic dissection tissues as compared with normal aortic tissues, and was associated with increased apoptotic SMCs and decreased AEG-1 expression. Mechanically, hypoxia promoted the expression of HIF-1a by PI3K-AKT pathway in HASMCs; HIF-1a further suppressed the expressions of AEG-1, a-SMA and SM22a, and promoted osteopontin (OPN) expression. Functionally, HIF-1a inhibited the proliferation and migration of HASMCs. However, si-HIF-1a or Akt inhibitor abrogated HIF-1a-mediated related expressions and biological effects above. In conclusion, HIF-1a induces HASMC phenotype switch, and closely related to PI3K/AKT and AEG-1 signaling, which may provide new avenues for the prevention and treatment of aortic dissection diseases.

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