Inhibitory Effects of CD99-derived Peptide CD99CRIII3 on the Extravasation of Monocytes and Inflammatory Reactions in Contact Dermatitis Mouse Model
1
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
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.
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.
참고문헌 (27)
- Leung DY, "Atopic dermatitis", Lancet, 361, pp.151~160 (2003)
- Giustizieri ML, "Keratinocytes from patients with atopic dermatitis and psoriasis show a distinct chemokine production profile in response to T cell-derived cytokines", J Allergy Clin Immunol, 107, pp.871~877 (2001)
- Leung DY, "New insights into atopic dermatitis", J Clin Invest, 113, pp.651~657 (2004)
- Nomura I, "Distinct patterns of gene expression in the skin lesions of atopic dermatitis and psoriasis: a gene microarray analysis", J Allergy Clin Immunol, 112, pp.1195~1202 (2003)
- Beresford L, "Nerve fibres are required to evoke a contact sensitivity response in mice", Immunology, 111, pp.118~125 (2004)
- Levy R, "A human thymus-leukemia antigen defined by hybridoma monoclonal antibodies", Proc Natl Acad Sci U S A, 76, pp.6552~6556 (1979)
- Waclavicek M, "CD99 engagement on human peripheral blood T cells results in TCR", CD3-dependent cellular activation and allows for Th1-restricted cytokine production, 1998, pp.161, 4671~4678
- Sohn HW, "CD99 regulates the transport of MHC class I molecules from the Golgi complex to the cell surface", J Immunol, 166, pp.787~794 (2001)
- Sciandra M, "CD99 drives terminal differentiation of osteosarcoma cells by acting as a spatial regulator of ERK 1", 2, 2014, pp.29, 1295~1309
- Sohn HW, "Engagement of CD99 induces apoptosis through a calcineurin-independent pathway in Ewing’s sarcoma cells", Am J Pathol, 153, pp.1937~1945 (1998)
- Husak Z, "Death induction by CD99 ligation in TEL", AML1-positive acute lymphoblastic leukemia and normal B cell precursors, 2010, pp.88, 405~412
- Husak Z, "CD99 ligation upregulates HSP70on acute lymphoblastic leukemia cells and concomitantly increases NK cytotoxicity", Cell Death Dis, 3, pp.e425~ (2012)
- Bernard A, "A T cell surface molecule different from CD2 is involved in spontaneous rosette formation with erythrocytes", J Immunol, 140, pp.1802~1807 (1988)
- Gelin C, "The E2 antigen, a 32 kd glycoprotein involved in T-cell adhesion processes, is the MIC2 gene product", EMBO J, 8, pp.3253~3259 (1989)
- Bernard G, "The E2 molecule (CD99) specifically triggers homotypic aggregation of CD4+ CD8+ thymocytes", J Immunol, 154, pp.26~32 (1995)
- Hahn JH, "CD99 (MIC2) regulates the LFA-1", ICAM-1-mediated adhesion of lymphocytes, and its gene encodes both positive and negative regulators of cellular adhesion, 1997, pp.159, 2250~2258
- Hahn MJ, "Differential activation of MAP kinase family members triggered by CD99 engagement", FEBS Lett, 470, pp.350~354 (2000)
- Lee KJ, "CD99-Derived Agonist Ligands Inhibit Fibronectin-Induced Activation of β1 Integrin through the Protein Kinase A", SHP2, PTPN12, pp.Focal Adhesion Kinase Signaling Pathway, Mol Cell Biol[DOI]
- Schenkel AR, "CD99 plays a major role in the migration of monocytes through endothelial junctions", Nat J Immunol, 3, pp.143~150 (2002)
- Lou O, "CD99 is a key mediator of the transendothelial migration of neutrophils", J Immunol, 178, pp.1136~1143 (2007)
- Bixel G, "Mouse CD99 participates in T-cell recruitment into inflamed skin", Blood, 104, pp.3205~3213 (2004)
- Byun HJ, "A splice variant of CD99 increases motility and MMP-9expression of human breast cancer cells through the AKT-, ERK-, and JNK-dependent AP-1 activation signaling pathways", J Biol Chem, 281, pp.34833~34847 (2006)
- Cotter TG, "A monoclonal antibodyinhibiting FMLP-induced chemotaxis of human neutrophils", J Immunol, 127, pp.2241~2245 (1981)
- Wu BC, "Mechanisms of the Innate Defense Regulator Peptide-1002 Anti-Inflammatory Activity in a Sterile Inflammation Mouse Model", J Immunol, 199, pp.3592~3603 (2017)
- Sahu RP, "Topical application of a platelet activating factor receptor agonist suppresses phorbol ester-induced acute and chronic inflammation and has cancer chemopreventive activity in mouse skin", PLoS One, 9, pp.e111608~ (2014)
- Kim MJ, "Elaeocarpusin Inhibits Mast Cell-Mediated Allergic Inflammation", Front Pharmacol, 9, pp.591~ (2018)
- Jang-Hee Hahn, "Paired Ig-Like Type 2 Receptor-Derived Agonist Ligands Ameliorate Inflammatory Reactions by Downregulating beta1 Integrin Activity", Molecules and Cells, 39(7), pp.557~565 (2016), 한국분자세포생물학회[DOI]
