Inhibitory Effects of CD99-derived Peptide CD99CRIII3 on the Extravasation of Monocytes and Inflammatory Reactions in Contact Dermatitis Mouse Model

Hyun-Mi Ju; Kyeong-Han Park

doi:10.11637/kjpa.2018.31.4.143

Journal List > Korean J Phys Anthropol > v.31(4) > 1110900

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Ju and Park: Inhibitory Effects of CD99-derived Peptide CD99CRIII3 on the Extravasation of Monocytes and Inflammatory Reactions in Contact Dermatitis Mouse Model

Original Article

Korean J Phys Anthropol 2018;31(4):143-149.

Published online: 20 April 2018

DOI: https://doi.org/10.11637/kjpa.2018.31.4.143

Inhibitory Effects of CD99-derived Peptide CD99CRIII3 on the Extravasation of Monocytes and Inflammatory Reactions in Contact Dermatitis Mouse Model

Hyun-Mi Ju, Kyeong-Han Park

Department of Anatomy and Cell Biology, School of Medicine, Kangwon National University

The author(s) agree to abide by the good publication practice guideline for medical journals. The author(s) declare that there are no conflicts of interest. Correspondence to: Kyeong-Han Park (Department of Anatomy and Cell Biology, School of Medicine, Kangwon National University) E-mail: insitu@kangwon.ac.kr

Received 4 October 2018 Revised 3 December 2018 Accepted 4 December 2018

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Leucocyte extravasation has been known to play an important role in inflammatory reactions including contact dermatitis. Previous studies suggested that CD99 regulates β1 integrin activity and may be a novel therapeutic target molecule for inflammatory diseases. In this study, the effects of CD99-derived peptide, CD99CRIII3, on inflammatory reactions in contact dermatitis mouse model were investigated. CD99CRIII3 decreased β1-integrin activity in human monocytic U937 cells. CD99CRIII3 inhibited the adhesion of U937 monocytes to human umbilical vein endothelial cells and their extravasation through human umbilical vein endothelial cells. CD99CRIII3 reduced inflammation in the phorbol myristate acetate-induced contact dermatitis mice in a dose-dependent manner. These results indicate that CD99CRIII3 suppresses the extravasation of monocytes and inflammatory reactions in the animal model of the contact dermatitis, suggesting that CD99CRIII3 could be a new drug candidate against inflammatory skin diseases.

Keywords: CD99-derived peptide, Contact dermatitis, CD99, Inflammation

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Fig. 1.

CD99CRIII3 inhibit β1-integrin activity in a dose depen-dent manner. U937 cells were treated with various amount of CD-99CRIII3 and then subjected to western blot analysis (A). Relative activity levels of β1-integrin in (A) are shown as relative intensity of bands by measuring with a densitometer (B).

Fig. 2.

Effects of CD99CRIII3 on cell-cell adhesion and transendothelial migration of monocytes. WEHI 274.1 monocytes were treated with CD99CRIII3 or control peptide and subjected to cell-cell binding assay (A) and were also subjected to transendothelial migration (B). Results are the mean± S.E. of triplicate assays: p<0.05 (∗), p<0.01 (∗∗), p<0.001 (∗∗∗).

Fig. 3.

CD99CRIII3 suppresses inflammatory reaction in a murine model of acute contact dermatitis. (A) After PMA-mediated induction of contact dermatitis in mice, CD99CRIII3 or control peptide were injected into tail vein of mice. After 6 h, vascular permeability was mea-sured by injection of Evans Blue dye and observed with the naked eye. (B) Ears were removed from the mice treated as described in Figure 3(A). After soaking in formamide solution overnight, the amount of Evan Blue leakage from the vessels was measured by a spectrophotom-eter. (C) Ear pieces were removed from mice treated as described in Figure 3(A), and the ear pieces weighed. Results are the mean± S.E. of triplicate cultures: p<0.05 (∗), p<0.01 (∗∗), p<0.001 (∗∗∗).

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