The Wound Healing Peptide, AES16-2M, Ameliorates Atopic Dermatitis In Vivo
- Authors
- Kim, Myun Soo; Song, Jisun; Park, Sunyoung; Kim, Tae Sung; Park, Hyun Jeong; Cho, Daeho
- Issue Date
- 2월-2021
- Publisher
- MDPI
- Keywords
- short peptide; AES16-2M; atopic dermatitis
- Citation
- MOLECULES, v.26, no.4
- Indexed
- SCIE
SCOPUS
- Journal Title
- MOLECULES
- Volume
- 26
- Number
- 4
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/49664
- DOI
- 10.3390/molecules26041168
- ISSN
- 1420-3049
- Abstract
- Peptide materials have recently been considered for use in various industrial fields. Because of their efficacy, safety, and low cost, therapeutic peptides are studied for various diseases, including atopic dermatitis (AD). AD is a common inflammatory skin disease impairing the patient's quality of life. Various therapies, such as treatments with corticosteroids, calcineurin inhibitors, and antibody drugs, have been applied, but numerous side effects have been reported, including skin atrophy, burning, and infection. In the case of antibody drugs, immunogenicity against the drugs can be a problem. To overcome these side effects, small peptides are considered therapeutic agents. We previously identified the small wound healing peptide AES16-2M with a sequence of REGRT, and examined its effects on AD in this study. Interestingly, the administration of AES16-2M downregulated the AD disease score, ear thickness, serum IgE, and thymic stromal lymphopoietin (TSLP) in AD mice. The thickness of the epidermal layer was also improved by AES16-2M treatment. In addition, quantities of IL-4-, IL-13-, and IL-17-producing CD4 T cells from peripheral lymph nodes and spleens were reduced by injection of AES16-2M. Furthermore, the expression of TSLP was significantly reduced in AES16-2M-treated human keratinocytes. Therefore, these results suggest that AES16-2M can be a novel candidate for AD treatment.
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Collections - College of Life Sciences and Biotechnology > Division of Life Sciences > 1. Journal Articles
- Graduate School > Department of Life Sciences > 1. Journal Articles
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