title: Reactive Oxygen Species Mediated Prostaglandin E2Contributes to Acute Response of Epithelial Injury.
abstract: 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 PGE2as 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 PGE2production 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 PGE2in human keratinocytes responding to mechanical injury in the acute phase.
authors.affiliation: Department 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; Department of Burns and Plastic Surgery, Guangzhou Red Cross Hospital, Jinan University, Guangzhou 510220, China.
authors.forename: Yi-Ping
authors.initials: YP
authors.lastname: Hu
authors.affiliation: Department 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.
authors.forename: Yin-Bo
authors.identifier: 0000-0002-2598-5884
authors.initials: YB
authors.lastname: Peng
authors.affiliation: Department 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.
authors.forename: Yi-Fan
authors.initials: YF
authors.lastname: Zhang
authors.affiliation: Department 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.
authors.forename: Ying
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department 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.
authors.forename: Wei-Rong
authors.initials: WR
authors.lastname: Yu
authors.affiliation: Department 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.
authors.forename: Min
authors.identifier: 0000-0002-6946-8766
authors.initials: M
authors.lastname: Yao
authors.affiliation: Department 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.
authors.forename: Xiu-Jun
authors.identifier: 0000-0002-8448-4932
authors.initials: XJ
authors.lastname: Fu
mesh_terms: D002460:Cell Line; D051545:Cyclooxygenase 1 / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism*; D004789:Enzyme Activation; D004848:Epithelium / Q000201:enzymology / Q000473:pathology*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D006801:Humans; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D017382:Reactive Oxygen Species; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; D048049:Extracellular Signal-Regulated MAP Kinases; D015232:Dinoprostone