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RETRACTED: Hypoxia-inducible factor 1a induces phenotype switch of human aortic vascular smooth muscle cell through PI3K/AKT/AEG-1 signaling (Retracted Article)
被引:51
|作者:
Liu, Kai
[1
]
Fang, Changcun
[1
]
Shen, Yuwen
[1
]
Liu, Zhengqin
[1
]
Zhang, Min
[1
]
Ma, Bingbing
[1
]
Pang, Xinyan
[1
]
机构:
[1] Shandong Univ, Qilu Hosp, Dept Cardiovasc Surg, Jinan 250012, Shandong, Peoples R China
来源:
关键词:
HIF-1;
alpha;
HASMC;
PI3K/AKT/AEG-1;
DOWN-REGULATION;
ANGIOTENSIN-II;
IN-VIVO;
DIFFERENTIATION;
PROLIFERATION;
REGULATOR;
DISEASE;
REPAIR;
D O I:
10.18632/oncotarget.16448
中图分类号:
R73 [肿瘤学];
学科分类号:
100214 ;
摘要:
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 HIF1a- 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 HIF1a 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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页码:33343 / 33352
页数:10
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