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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 4123854, 8 pages
Research Article

Reactive Oxygen Species Mediated Prostaglandin E2 Contributes to Acute Response of Epithelial Injury

1Department of Burns and Plastic Surgery, No. 9 People’s Hospital, and Institute of Traumatic Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai 201900, China
2Department of Burns and Plastic Surgery, Guangzhou Red Cross Hospital, Jinan University, Guangzhou 510220, China

Correspondence should be addressed to Xiu-Jun Fu

Received 22 October 2016; Revised 20 December 2016; Accepted 28 December 2016; Published 9 February 2017

Academic Editor: Liang-Jun Yan

Copyright © 2017 Yi-Ping Hu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Reactive oxygen species (ROS) generated after tissue injury play a crucial role during wound healing through initiating acute inflammation, clarifying infection and dead tissue, and mediating various intracellular signal transduction. Prostaglandin E2 (PGE2) has been identified as one of the major factors responsible for inflammation and tissue repair. In this study, we tested our hypothesis that ROS produced by damaged human keratinocytes induces the synthesis of PGE2. In vitro epithelial wounding model was used to observe the production of ROS and secretion of PGE2 as well as the involved signal pathway. The mechanical injury caused the rapid production of ROS in in vitro cultured keratinocytes, which was significantly blocked by an inhibitor of nicotinamide adenine dinucleotide phosphate oxidase. The increased intracellular ROS caused by mechanical injury stimulates PGE2 production in a time-dependent manner via the activation of cyclooxygenase-2 (COX-2), which was stimulated by phosphorylation of extracellular signal-regulated protein kinase (ERK). These results indicate ROS-induced ERK activation leading to the activation of COX-2 and the synthesis of PGE2 in human keratinocytes responding to mechanical injury in the acute phase.