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- W2790082110 abstract "Individuals exposed to long-term spaceflight often experience cardiovascular dysfunctions characterized by orthostatic intolerance, disability on physical exercise, and even frank syncope. Recent studies have showed that the alterations of cardiovascular system are closely related to the functional changes of endothelial cells. We have shown previously that autophagy can be induced by simulated microgravity in human umbilical vein endothelial cells (HUVECs). However, the mechanism of enhanced autophagy induced by simulated microgravity and its role in the regulation of endothelial function still remain unclear. We report here that 48 h clinorotation promoted cell migration in HUVECs by induction of autophagy. Furthermore, clinorotation enhanced autophagy by the mechanism of human murine double minute 2 (HDM2)-dependent degradation of cytoplasmic p53 at 26S proteasome, which results in the suppression of mechanistic target of rapamycin (mTOR), but not via activation of AMPK in HUVECs. These results support the key role of HDM2-p53 in direct downregulation of mTOR, but not through AMPK in microgravity-induced autophagy in HUVECs." @default.
- W2790082110 created "2018-03-29" @default.
- W2790082110 creator A5000406335 @default.
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- W2790082110 date "2018-02-02" @default.
- W2790082110 modified "2023-10-12" @default.
- W2790082110 title "Clinorotation-induced autophagy via HDM2-p53-mTOR pathway enhances cell migration in vascular endothelial cells" @default.
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- W2790082110 doi "https://doi.org/10.1038/s41419-017-0185-2" @default.
- W2790082110 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5833810" @default.
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- W2790082110 hasPublicationYear "2018" @default.
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