Biphasic effects of autophagy on decompression bubble-induced endothelial injury
Endothelial dysfunction induced by bubbles plays an important role in decompression sickness (DCS), but the mechanism of which has not been clear. The present study was to investigate the role of autophagy in bubble-induced endothelial injury. Human umbilical vein endothelial cells (HUVECs) were tre...
| Main Authors: | , , , , , , , |
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| Format: | Journal Article |
| Language: | English |
| Published: |
WILEY
2019
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| Online Access: | http://creativecommons.org/licenses/by/4.0/ http://hdl.handle.net/20.500.11937/79637 |
| _version_ | 1848764088603115520 |
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| author | Wang, M. Zhang, K. Nie, S. Huang, G. Yi, H. He, C. Buzzacott, Peter Xu, W. |
| author_facet | Wang, M. Zhang, K. Nie, S. Huang, G. Yi, H. He, C. Buzzacott, Peter Xu, W. |
| author_sort | Wang, M. |
| building | Curtin Institutional Repository |
| collection | Online Access |
| description | Endothelial dysfunction induced by bubbles plays an important role in decompression sickness (DCS), but the mechanism of which has not been clear. The present study was to investigate the role of autophagy in bubble-induced endothelial injury. Human umbilical vein endothelial cells (HUVECs) were treated with bubbles, autophagy markers and endothelial injury indices were determined, and relationship strengths were quantified. Effects of autophagy inhibitor 3-methyladenine (3-MA) were observed. Bubble contact for 1, 5, 10, 20 or 30 minutes induced significant autophagy with increases in LC3-II/I ratio and Beclin-1, and a decrease in P62, which correlated with bubble contact duration. Apoptosis rate, cytochrome C and cleaved caspase-3 increased, and cell viability decreased following bubble contact for 10, 20 or 30 minutes, but not for 1 or 5 minutes. Injuries in HUVECs were correlated with LC3-II/I ratio and partially reversed by 3-MA in 10, 20 or 30 minutes contact, but worsened in 1 or 5 minutes. Bubble pre-conditioning for 1 minutes resulted in increased cell viability and decreased apoptosis rate compared with no pre-conditioning, and 30-minutes pre-conditioning induced opposing changes, all of which were inhibited by 3-MA. In conclusion, autophagy was involved and played a biphasic role in bubble-induced endothelial injury. |
| first_indexed | 2025-11-14T11:13:48Z |
| format | Journal Article |
| id | curtin-20.500.11937-79637 |
| institution | Curtin University Malaysia |
| institution_category | Local University |
| language | English |
| last_indexed | 2025-11-14T11:13:48Z |
| publishDate | 2019 |
| publisher | WILEY |
| recordtype | eprints |
| repository_type | Digital Repository |
| spelling | curtin-20.500.11937-796372020-06-23T00:34:17Z Biphasic effects of autophagy on decompression bubble-induced endothelial injury Wang, M. Zhang, K. Nie, S. Huang, G. Yi, H. He, C. Buzzacott, Peter Xu, W. Science & Technology Life Sciences & Biomedicine Cell Biology Medicine, Research & Experimental Research & Experimental Medicine autophagy bubble decompression sickness endothelial cell IN-VITRO MODULATING AUTOPHAGY PROLIFERATION INHIBITION SICKNESS Endothelial dysfunction induced by bubbles plays an important role in decompression sickness (DCS), but the mechanism of which has not been clear. The present study was to investigate the role of autophagy in bubble-induced endothelial injury. Human umbilical vein endothelial cells (HUVECs) were treated with bubbles, autophagy markers and endothelial injury indices were determined, and relationship strengths were quantified. Effects of autophagy inhibitor 3-methyladenine (3-MA) were observed. Bubble contact for 1, 5, 10, 20 or 30 minutes induced significant autophagy with increases in LC3-II/I ratio and Beclin-1, and a decrease in P62, which correlated with bubble contact duration. Apoptosis rate, cytochrome C and cleaved caspase-3 increased, and cell viability decreased following bubble contact for 10, 20 or 30 minutes, but not for 1 or 5 minutes. Injuries in HUVECs were correlated with LC3-II/I ratio and partially reversed by 3-MA in 10, 20 or 30 minutes contact, but worsened in 1 or 5 minutes. Bubble pre-conditioning for 1 minutes resulted in increased cell viability and decreased apoptosis rate compared with no pre-conditioning, and 30-minutes pre-conditioning induced opposing changes, all of which were inhibited by 3-MA. In conclusion, autophagy was involved and played a biphasic role in bubble-induced endothelial injury. 2019 Journal Article http://hdl.handle.net/20.500.11937/79637 10.1111/jcmm.14672 English http://creativecommons.org/licenses/by/4.0/ WILEY fulltext |
| spellingShingle | Science & Technology Life Sciences & Biomedicine Cell Biology Medicine, Research & Experimental Research & Experimental Medicine autophagy bubble decompression sickness endothelial cell IN-VITRO MODULATING AUTOPHAGY PROLIFERATION INHIBITION SICKNESS Wang, M. Zhang, K. Nie, S. Huang, G. Yi, H. He, C. Buzzacott, Peter Xu, W. Biphasic effects of autophagy on decompression bubble-induced endothelial injury |
| title | Biphasic effects of autophagy on decompression bubble-induced endothelial injury |
| title_full | Biphasic effects of autophagy on decompression bubble-induced endothelial injury |
| title_fullStr | Biphasic effects of autophagy on decompression bubble-induced endothelial injury |
| title_full_unstemmed | Biphasic effects of autophagy on decompression bubble-induced endothelial injury |
| title_short | Biphasic effects of autophagy on decompression bubble-induced endothelial injury |
| title_sort | biphasic effects of autophagy on decompression bubble-induced endothelial injury |
| topic | Science & Technology Life Sciences & Biomedicine Cell Biology Medicine, Research & Experimental Research & Experimental Medicine autophagy bubble decompression sickness endothelial cell IN-VITRO MODULATING AUTOPHAGY PROLIFERATION INHIBITION SICKNESS |
| url | http://creativecommons.org/licenses/by/4.0/ http://hdl.handle.net/20.500.11937/79637 |