Biphasic Effects of Autophagy on Decompression Bubble-induced Endothelial Injury

Overview

Journal J Cell Mol Med

Specialties Cell Biology
Molecular Biology

Date 2019 Sep 14

PMID 31515946

Citations 2

Authors

Mengmeng Wang

Kun Zhang

Shaojie Nie

Guoyang Huang

Hongjie Yi

Chunyang He

Peter Buzzacott

Weigang Xu

Affiliations

Soon will be listed here.

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.

Citing Articles

The involvement of transient receptor potential channels in mast cell activation by microbubbles.

Liu J, Qing L, He Y, Zhu Q, Xu W, Wu J J Cell Mol Med. 2023; 27(22):3628-3636.

PMID: 37680043 PMC: 10660621. DOI: 10.1111/jcmm.17947.

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

Wang M, Zhang K, Nie S, Huang G, Yi H, He C J Cell Mol Med. 2019; 23(12):8058-8066.

PMID: 31515946 PMC: 6850936. DOI: 10.1111/jcmm.14672.

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