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  • Title: Hypoxia-induced autophagy in endothelial cells: a double-edged sword in the progression of infantile haemangioma?
    Author: Chen G, Zhang W, Li YP, Ren JG, Xu N, Liu H, Wang FQ, Sun ZJ, Jia J, Zhao YF.
    Journal: Cardiovasc Res; 2013 Jun 01; 98(3):437-48. PubMed ID: 23408345.
    Abstract:
    AIMS: The aim of this study was to investigate the precise role of hypoxia-induced autophagy in endothelial cells, and whether it contributes to the distinctive progression of infantile haemangioma (IH). METHODS AND RESULTS: The endothelial cells (EOMA and HUVECs) were cultured under hypoxic conditions for indicated times (0-72 h). The results showed that short exposure of the endothelial cells to hypoxia resulted in increased cell survival and proliferation, accompanied by occurrence of autophagy. Prolonged hypoxia-induced autophagy, correlating with increased cell death, was also detected afterwards. Correspondingly, autophagy inhibition prevented the enhanced cell survival and proliferation capacity, advanced the occurrence of cell-death in early hypoxic stage, and meanwhile attenuated the ability of prolonged hypoxia in cell-death induction. Moreover, our data demonstrated that the functional transformation of hypoxia-induced autophagy, pro-survival to pro-death, was rigorously regulated by the switch between hypoxia-inducible factor-1α (HIF-1α) and mammalian target of rapamycin (mTOR) pathways. Importantly, we also revealed the activation levels of HIF-1α and mTOR, as well as the autophagy status during the progression of IH. CONCLUSION: This study unmasks the functional switch between HIF-1α and mTOR in regulating hypoxia-induced autophagy in endothelial cells and, more importantly, indicates its potential role in the progression of IH.
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