PEP-1-PEA15 suppresses inflammatory responses by regulation of MAPK in macrophages and animal models
- Authors
- Yong, Ji In; Kim, Dae Won; Shin, Min Jea; Jo, Hyo Sang; Park, Jung Hwan; Cho, Su Bin; Lee, Chi Hem; Yeo, Hyeon Ji; Yeo, Eun Ji; Choi, Yeon Joo; Kim, Ji An; Hwang, Jung Soon; Kim, Duk-Soo; Kim, Hyun Ah; Cho, Yong-Jun; Lee, Keun Wook; Han, Kyu Hyung; Park, Jinseu; Eum, Won Sik; Choi, Soo Young
- Issue Date
- Nov-2018
- Publisher
- Elsevier BV
- Keywords
- PEP-1-PEA15; Inflammation; MAPK; Cytokines; Protein therapy
- Citation
- Immunobiology, v.223, no.11, pp 709 - 717
- Pages
- 9
- Journal Title
- Immunobiology
- Volume
- 223
- Number
- 11
- Start Page
- 709
- End Page
- 717
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/5548
- DOI
- 10.1016/j.imbio.2018.07.019
- ISSN
- 0171-2985
- Abstract
- Phosphoprotein enriched in astrocytes 15 (PEA15) plays a multi-functional role in neuronal cell survival, however the effects of PEA15 against inflammation have not been investigated yet. To examine the effects of PEP-1-PEA15 protein against lipopolysaccharide (LPS)-induced inflammatory responses in Raw 264.7 cells and in a 12-O-tetradecanoylphobol 13-acetate (TPA)-induced mouse model, we constructed and purified PEP-1-PEA15 protein, which can transduce into cells or tissues. PEP-1-PEA15 inhibited LPS-induced damage in cells including that caused by reactive oxygen species (ROS) production and DNA fragmentation. PEP-1-PEA15 also significantly suppressed activation of mitogen activated protein kinases (MAPKs), pro-inflammatory mediator proteins and various cytokines. In a TPA-induced mouse ear edema model, PEP-1-PEA15 significantly reduced ear weight and thickness as well as MAPK activation as well as the expression levels of COX-2, iNOS, IL-6, IL-1 beta, and TNF-alpha. These results demonstrated that PEP-1-PEA15 showed anti-inflammatory effect in cells and animal model suggesting that this fusion protein protects cells or skin tissues from inflammatory response.
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Collections - College of Medicine > Department of Anatomy > 1. Journal Articles
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