The activation of CD99 inhibits cell-extracellular matrix adhesion by suppressing β1 integrin affinity
2
조회
0
다운로드
1
인용
0
참고문헌
키워드
초록
CD99 is known to be involved in the regulation of cell-cell adhesion. However, it remains unclear whether CD99 controls cell-extracellular matrix adhesion. In this study, the effects of CD99 activation on cell-extracellular matrix adhesion were investigated. It was found that engagement of CD99 with the stimulating antibody YG32 downregulated the adhesion of MCF-7 cells to fibronectin, laminin and collagen IV in a dose-dependent manner. The CD99 effect on cell-ECM adhesion was inhibited by overexpression of the dominant negative form of CD99 or CD99 siRNA transfection. Treatment of cells with Mn2+ or by β1 integrin-stimulating antibody restored the inhibitory effect of CD99 on cell-ECM adhesion. Cross-linking CD99 inactivated β1 integrin through conformational change. CD99 activation caused dephosphorylation at Tyr-397 in FAK,which was restored by the β1 stimulating antibody. Taken together,these results provide the first evidence that CD99 inhibits cell-extracellular matrix adhesion by suppressing β1 integrin affinity. [BMB reports 2012; 45(3): 159-164]
Abstract
CD99 is known to be involved in the regulation of cell-cell adhesion. However, it remains unclear whether CD99 controls cell-extracellular matrix adhesion. In this study, the effects of CD99 activation on cell-extracellular matrix adhesion were investigated. It was found that engagement of CD99 with the stimulating antibody YG32 downregulated the adhesion of MCF-7 cells to fibronectin, laminin and collagen IV in a dose-dependent manner. The CD99 effect on cell-ECM adhesion was inhibited by overexpression of the dominant negative form of CD99 or CD99 siRNA transfection. Treatment of cells with Mn2+ or by β1 integrin-stimulating antibody restored the inhibitory effect of CD99 on cell-ECM adhesion. Cross-linking CD99 inactivated β1 integrin through conformational change. CD99 activation caused dephosphorylation at Tyr-397 in FAK,which was restored by the β1 stimulating antibody. Taken together,these results provide the first evidence that CD99 inhibits cell-extracellular matrix adhesion by suppressing β1 integrin affinity. [BMB reports 2012; 45(3): 159-164]
참고문헌 (36)
- Sixt, M., "Beta1 integrins: zip codes and signaling relay forblood cells", Curr. Opin. Cell Biol., 18, pp.482~490 (2006)
- Al-Jamal, R., "Beta1 integrin in tissue remodelling and repair: from phenomena to concepts", Pharmacol. Ther., 120, pp.81~101 (2008)
- Wang, X. Q., "The thrombospondin receptor CD47 (IAP) modulates and associates with alpha2 beta1 integrin in vascular smooth muscle cells", Mol. Biol. Cell, 9, pp.865~874 (1998)
- Fenczik, C. A., "Complementation of dominant suppression implicates CD98 in integrin activation", Nature, 390, pp.81~85 (1997)
- Sun-Mi Kim, "CD98 activation increases surface expression and clusteringof β1 integrins in MCF-7 cells through FAK", Src- andcytoskeleton-independent mechanisms, 2008, pp.40(3), 261~270[DOI]
- Kotha, J., "Tetraspanin CD9 regulates beta 1 integrin activationand enhances cell motility to fibronectin via a PI-3 kinase-dependent pathway", Exp. Cell Res., 314, pp.1811~1822 (2008)
- Nishiuchi, R., "Potentiation of the ligand-binding activity of integrin alpha3beta1 via association with tetraspanin CD151", PNAS, 102, pp.1939~1944 (2005)
- Serru, V., "Selective tetraspan- integrin complexes (CD81", alpha4beta1, CD151, alpha6beta1) under conditions disrupting tetraspan interactions, pp.Biochem. J., 1999[DOI]
- Oinuma, I., "Semaphorin4D", Plexin-B1-mediated R-Ras GAP activity inhibits cellmigration by regulating beta(1) integrin activity, 2006, pp.173, 601~613
- Oinuma, I., "The Semaphorin 4D receptor Plexin-B1 is a GTPase activating protein for R-Ras", Science, 305, pp.862~865 (2004)
- Miao, H., "Activation of EphA2 kinase suppresses integrinfunction and causes focal-adhesion-kinase dephosphorylation", Nat. Cell Biol., 2, pp.62~69 (2000)
- Levy, R., "A human thymus-leukemia antigen defined by hybridoma monoclonal antibodies", Proc. Natl. Acad. Sci. U.S.A., 76, pp.6552~6556 (1979)
- Hahn J. H., "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
- Schön, M., "Mucosal T lymphocyte numbers are selectively reduced in integrin alpha E (CD103)-deficient mice", J. Immunol., 162, pp.6641~6649 (1999)
- Schenkel, A., "CD99 plays a major role in the migration of monocytes through endothelial junctions", Nat. Immunol., 2, pp.143~150 (2002)
- Wingett, D., "A role for CD99 in T cell activation", Cell Immunol., 193, pp.17~23 (1999)
- Pettersen, R., "CD99 signals caspase-independent T cell death", J. Immunol., 166, pp.4931~4942 (2001)
- Sohn, H. W., "Engagement of CD99 induces apoptosis through a calcineurin-independent pathway in Ewing's sarcoma cells", Am. J. Pathol., 153, pp.1937~1945 (1998)
- Schenkel, A. R., "CD99 plays a major role in the migration of monocytes through endothelial junctions", Nat. Immunol., 3, pp.143~150 (2002)
- Dustin, M. L., "T-cell receptor cross-linking transiently stimulates adhesiveness through LFA-1", Nature, 341, pp.619~624 (1989)
- Bernard, G., "CD99 (E2) up-regulates alpha4beta1-dependent T cell adhesion to inflamed vascular endothelium under flow conditions", Eur. J. Immunol., 30, pp.3061~3065 (2000)
- Alberti, I., "CD99 isoforms expression dictates T cell functional outcomes", FASEB J., 16, pp.1946~1948 (2002)
- Hahn, M. J., "Differential activation of MAP kinase family members triggered by CD99 engagement", FEBS Lett., 470, pp.350~354 (2000)
- Ni, H., "Integrin activation by dithiothreitol or Mn2+ induces a ligand- occupied conformation and exposure of a novel NH2-terminal regulatory site on the beta1 integrin chain", J. Biol. Chem., 273, pp.7981~7987 (1998)
- Dransfield, I., "Regulated expression of Mg2+ binding epitope on leukocyte integrin alpha subunits", EMBO J., 8, pp.3759~3765 (1989)
- Mitra, S. K., "Integrin-regulated FAK-Src signaling in normal and cancer cells", Curr. Opin. Cell. Biol., 18, pp.516~523 (2006)
- Lee, H. A., "Metastasis Suppressor KAI1", CD82 Attenuates the Matrix Adhesion of Human Prostate Cancer Cells by Suppressing Fibronectin Expression and beta(1) Integrin Activation, 2011, pp.27(5), 575~586[DOI]
- Maione, F., "Semaphorin 3A is an endogenous angiogenesis inhibitor that blocks tumor growth and normalizes tumor vasculature in transgenic mouse models", J. Clin Invest, 119, pp.3356~3372 (2009)
- Bourgin, C., "The EphA4 receptor regulates dendritic spine remodelingby affecting beta1-integrin signaling pathways", J.Cell. Biol., 178, pp.1295~1307 (2007)
- Dail, M., "Eph receptors inactivate R-Ras through differentmechanisms to achieve cell repulsion", J. Cell. Science, 119, pp.1244~1254 (2005)
- Dufour, E. M., "CD99 is essential for leukocyte diapedesis in vivo", Cell. Commun. Adhes., 15, pp.351~363 (2008)
- Lou, O., "CD99 is a key mediator of the transendothelial migrationof neutrophils", J. Immunol., 178, pp.1136~1143 (2007)
- Imbert, A. M., "CD99 expressed on human mobilized peripheral blood CD34+ cells is involved in transendothelial migration", Blood, 108, pp.2578~2586 (2006)
- Bixel, M. G., "CD99 and CD99L2 act at the same site as, but independently of, PECAM-1 during leukocyte diapedesis", Blood, 116, pp.1172~1184 (2010)
- Bixel, M. G., "A CD99-related antigen on endothelial cells mediates neutrophil but not lymphocyte extravasation in vivo", Blood, 109, pp.5327~5336 (2007)
- 이경진, "Ox-LDL suppresses PMA-induced MMP-9 expression and activity through CD36-mediated activation of PPAR-γ", Experimental and Molecular Medicine, 36(6), pp.534~544 (2004), 생화학분자생물학회