Journalartikel
Autorenliste: Wygrecka, Malgorzata; Marsh, Leigh M.; Morty, Rory E.; Henneke, Ingrid; Guenther, Andreas; Lohmeyer, Juergen; Markart, Philipp; Preissner, Klaus T.
Jahr der Veröffentlichung: 2009
Seiten: 5588-5598
Zeitschrift: Blood
Bandnummer: 113
Heftnummer: 22
ISSN: 0006-4971
eISSN: 1528-0020
Open Access Status: Bronze
DOI Link: https://doi.org/10.1182/blood-2008-08-170837
Verlag: American Society of Hematology (ASH Publications)
Abstract:
Cell surface-associated proteolysis plays a crucial role in the migration of mononuclear phagocytes to sites of inflammation. The glycolytic enzyme enolase-1 (ENO-1) binds plasminogen at the cell surface, enhancing local plasmin production. This study addressed the role played by ENO-1 in lipopolysaccharide (LPS) driven chemokine-directed monocyte migration and matrix invasion in vitro, as well as recruitment of monocytes to the alveolar compartment in vivo. LPS rapidly up-regulated ENO-1 cell-surface expression on human blood monocytes and U937 cells due to protein translocation from cytosolic pools, which increased plasmin generation, enhanced monocyte migration through epithelial monolayers, and promoted matrix degradation. These effects were abrogated by antibodies directed against the plasminogen binding site of ENO-1. Overexpression of ENO-1 in U937 cells increased their migratory and matrix-penetrating capacity, which was suppressed by overexpression of a truncated ENO-1 variant lacking the plasminogen binding site (ENO-1 Delta PLG). In vivo, intratracheal LPS application in mice promoted alveolar recruitment of monocytic cells that overexpressed ENO-1, but not of cells overexpressing ENO-1 Delta PLG. Consistent with these data, pneumonia-patients exhibited increased ENO-1 cell-surface expression on blood monocytes and intense ENO-1 staining of mononuclear cells in the alveolar space. These data suggest an important mechanism of inflammatory cell invasion mediated by increased cell-surface expression of ENO-1. (Blood. 2009; 113: 5588-5598)
Zitierstile
Harvard-Zitierstil: Wygrecka, M., Marsh, L., Morty, R., Henneke, I., Guenther, A., Lohmeyer, J., et al. (2009) Enolase-1 promotes plasminogen-mediated recruitment of monocytes to the acutely inflamed lung, Blood, 113(22), pp. 5588-5598. https://doi.org/10.1182/blood-2008-08-170837
APA-Zitierstil: Wygrecka, M., Marsh, L., Morty, R., Henneke, I., Guenther, A., Lohmeyer, J., Markart, P., & Preissner, K. (2009). Enolase-1 promotes plasminogen-mediated recruitment of monocytes to the acutely inflamed lung. Blood. 113(22), 5588-5598. https://doi.org/10.1182/blood-2008-08-170837
Schlagwörter
ALPHA-ENOLASE; ANNEXIN-II; CELL-SURFACE; FIBRINOLYTIC COMPONENTS; FOAM CELL; HISTONE H2B; HUMAN PERIPHERAL MONOCYTES; INDUCED MIGRATION; MATRIX INVASION