Literature DB >> 10088596

The cell biology of leukocyte-mediated proteolysis.

C A Owen1, E J Campbell.   

Abstract

Leukocyte-derived proteinases have the capacity to degrade every component of the extracellular matrix, and thereby play fundamental roles in physiological processes. However, if the activity of these proteinases is uncontrolled or dysregulated, they have the capacity to contribute to tissue injury that potentially affects every organ in the body. Although there is a substantial literature on structure and activity of these proteinases when they are free in solution, until recently there has been little information about the cell biology of proteinases and their inhibitors. Recent studies, however, have identified several mechanisms by which inflammatory cells can degrade extracellular proteins in a milieu that contains high-affinity proteinase inhibitors.

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Year:  1999        PMID: 10088596     DOI: 10.1002/jlb.65.2.137

Source DB:  PubMed          Journal:  J Leukoc Biol        ISSN: 0741-5400            Impact factor:   4.962


  111 in total

Review 1.  Regulation of tissue injury responses by the exposure of matricryptic sites within extracellular matrix molecules.

Authors:  G E Davis; K J Bayless; M J Davis; G A Meininger
Journal:  Am J Pathol       Date:  2000-05       Impact factor: 4.307

2.  Disaccharides generated from heparan sulphate or heparin modulate chemokine-induced T-cell adhesion to extracellular matrix.

Authors:  R Hershkoviz; H Schor; A Ariel; I Hecht; I R Cohen; O Lider; L Cahalon
Journal:  Immunology       Date:  2000-01       Impact factor: 7.397

3.  Matrix metalloproteinase expression correlates with virulence following neurotropic mouse hepatitis virus infection.

Authors:  Jiehao Zhou; Stephen A Stohlman; Roscoe Atkinson; David R Hinton; Norman W Marten
Journal:  J Virol       Date:  2002-08       Impact factor: 5.103

4.  Modulation of macrophage activity by proteolytic enzymes. Differential regulation of IL-6 and reactive oxygen intermediates (ROIs) synthesis as a possible homeostatic mechanism in the control of inflammation.

Authors:  K Bryniarski; K Maresz; M Szczepanik; M Ptak; W Ptak
Journal:  Inflammation       Date:  2003-12       Impact factor: 4.092

5.  Anaplasma phagocytophilum infection induces protracted neutrophil degranulation.

Authors:  Kyoung-seong Choi; Dennis J Grab; J Stephen Dumler
Journal:  Infect Immun       Date:  2004-06       Impact factor: 3.441

Review 6.  Neutrophil elastase, proteinase 3, and cathepsin G as therapeutic targets in human diseases.

Authors:  Brice Korkmaz; Marshall S Horwitz; Dieter E Jenne; Francis Gauthier
Journal:  Pharmacol Rev       Date:  2010-12       Impact factor: 25.468

7.  Neutrophils Oppose Uterine Epithelial Carcinogenesis via Debridement of Hypoxic Tumor Cells.

Authors:  Adam Blaisdell; Amandine Crequer; Devin Columbus; Takiko Daikoku; Khush Mittal; Sudhansu K Dey; Adrian Erlebacher
Journal:  Cancer Cell       Date:  2015-12-14       Impact factor: 31.743

Review 8.  Neutrophil proteinase 3 and dipeptidyl peptidase I (cathepsin C) as pharmacological targets in granulomatosis with polyangiitis (Wegener granulomatosis).

Authors:  Brice Korkmaz; Adam Lesner; Stephanie Letast; Yassir K Mahdi; Marie-Lise Jourdan; Sandrine Dallet-Choisy; Sylvain Marchand-Adam; Christine Kellenberger; Marie-Claude Viaud-Massuard; Dieter E Jenne; Francis Gauthier
Journal:  Semin Immunopathol       Date:  2013-02-06       Impact factor: 9.623

9.  Suppression of matrix metalloproteinase-9 transcription by transforming growth factor-beta is mediated by a nuclear factor-kappaB site.

Authors:  Kenji Ogawa; Feifei Chen; Chenzhong Kuang; Yan Chen
Journal:  Biochem J       Date:  2004-07-15       Impact factor: 3.857

10.  Role of neutrophil elastase in LTB4-induced neutrophil transmigration in vivo assessed with a specific inhibitor and neutrophil elastase deficient mice.

Authors:  R E Young; M-B Voisin; S Wang; J Dangerfield; S Nourshargh
Journal:  Br J Pharmacol       Date:  2007-04-30       Impact factor: 8.739

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