Original Article

Journal of Investigative Dermatology (1996) 106, 538–543; doi:10.1111/1523-1747.ep12343953

Interactions of Immature Human Mast Cells with Extracellular Matrix: Expression of Specific Adhesion Receptors and Their Role in Cell Binding to Matrix Proteins

Sabine Krüger-Krasagakes, Andreas Grützkau, Razmik Baghramian and Beate M Henz

Department of Dermatology, Virchow Klinikum, Humboldt Universität zu Berlin, Berlin, Germany

Received 24 August 1995; Revised 8 November 1995; Accepted 14 November 1995.

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Abstract

Interactions of cells with their extracellular matrix (ECM) are central to tissue-specific migration, localization, and function of migratory cells. Since mast cells circulate as immature precursor cells and home to tissues in a characteristic distribution, with increases in various disease states, we used the immature human mast cell line HMC-1 as a model to investigate the poorly understood mast cell-ECM interactions in humans. Functional adhesion studies showed that HMC-1 cells spontaneously adhere to fibronectin and laminin (80% at 6 and 12 mug/ml, respectively) and to collagen type I and III (50% at 20 mug/ml), whereas binding to vitronectin and collagen type IV required cell activation by phorbol myristate acetate. HMC-1 cells did not adhere to hyaluronic acid. Moreover, both fibronectin and laminin supported pronounced cytoplasmatic spreading with formation of isolated lamellipodia, whereas these cells exhibited a round cell shape on collagen and vitronectin, as shown by scanning electron microscopy. On flow cytometric analysis, HMC-1 cells expressed several adhesion molecules including the integrins beta1, alpha2 through alpha6, alphav, and alphavbeta5, as well as CD44. Adhesion to fibronectin and vitronectin was found to be divalent cation- and arginine-glycine-aspartic acid-dependent, and could be blocked by antibodies to beta 1 or alpha5, and alphav or alphavbeta5, respectively. In contrast, binding to laminin and collagen could not be blocked by monoclonal antibodies to any of the cell surface adhesion receptors expressed. Our results show that immature mast cells are able to modify their adhesive behavior in response to various ECM proteins and activating stimuli, and that this phenomenon is partly integrin mediated. These findings may be important for our understanding of the mechanisms leading to tissue-specific localization of mast cells.

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