Biphasic effects of autophagy on decompression bubble-induced endothelial injury

Mengmeng Wang, Kun Zhang, Shaojie Nie, Guoyang Huang, Hongjie Yi, Chunyang He, Peter Buzzacott, Weigang Xu

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish
JournalJournal of Cellular and Molecular Medicine
DOIs
Publication statusE-pub ahead of print - 12 Sep 2019

Fingerprint

Autophagy
Decompression
Wounds and Injuries
Human Umbilical Vein Endothelial Cells
Cell Survival
Apoptosis
Decompression Sickness
Cytochromes
Caspase 3
3-methyladenine

Cite this

Wang, Mengmeng ; Zhang, Kun ; Nie, Shaojie ; Huang, Guoyang ; Yi, Hongjie ; He, Chunyang ; Buzzacott, Peter ; Xu, Weigang. / Biphasic effects of autophagy on decompression bubble-induced endothelial injury. In: Journal of Cellular and Molecular Medicine. 2019.
@article{155e57787e7648f3899b701a0231ee40,
title = "Biphasic effects of autophagy on decompression bubble-induced endothelial injury",
abstract = "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.",
keywords = "autophagy, bubble, decompression sickness, endothelial cell",
author = "Mengmeng Wang and Kun Zhang and Shaojie Nie and Guoyang Huang and Hongjie Yi and Chunyang He and Peter Buzzacott and Weigang Xu",
year = "2019",
month = "9",
day = "12",
doi = "10.1111/jcmm.14672",
language = "English",
journal = "Journal of Cellular and Molecular Medicine",
issn = "1582-1838",
publisher = "Wiley-Blackwell",

}

Biphasic effects of autophagy on decompression bubble-induced endothelial injury. / Wang, Mengmeng; Zhang, Kun; Nie, Shaojie; Huang, Guoyang; Yi, Hongjie; He, Chunyang; Buzzacott, Peter; Xu, Weigang.

In: Journal of Cellular and Molecular Medicine, 12.09.2019.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Biphasic effects of autophagy on decompression bubble-induced endothelial injury

AU - Wang, Mengmeng

AU - Zhang, Kun

AU - Nie, Shaojie

AU - Huang, Guoyang

AU - Yi, Hongjie

AU - He, Chunyang

AU - Buzzacott, Peter

AU - Xu, Weigang

PY - 2019/9/12

Y1 - 2019/9/12

N2 - 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.

AB - 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.

KW - autophagy

KW - bubble

KW - decompression sickness

KW - endothelial cell

UR - http://www.scopus.com/inward/record.url?scp=85073804396&partnerID=8YFLogxK

U2 - 10.1111/jcmm.14672

DO - 10.1111/jcmm.14672

M3 - Article

JO - Journal of Cellular and Molecular Medicine

JF - Journal of Cellular and Molecular Medicine

SN - 1582-1838

ER -