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Dual targets for mouse mast cell protease-4 in mediating tissue damage in experimental bullous pemphigoid
Journal of Biological Chemistry. 2011;286(43):37358-37367.Abstract
Mouse mast cell protease-4 (mMCP-4) has been linked to autoimmune and inflammatory diseases, although the exact mechanisms underlying its role in these pathological conditions remain unclear. Here, we have found that mMCP-4 is critical in a mouse model of the autoimmune skin blistering disease bullous pemphigoid (BP). Mice lacking mMCP-4 were resistant to experimental BP. Complement activation, mast cell (MC) degranulation, and the early phase of neutrophil (PMN) recruitment occurred comparably in mMCP-4 -/- andWTmice. However, without mMCP-4, activation of matrix metalloproteinase (MMP)-9 was impaired in cultured mMCP-4 -/- MCs and in the skin of pathogenic IgG-injected mMCP-4 -/- mice. MMP-9 activation was not fully restored by local reconstitution with WT or mMCP-4 -/- PMNs. Local reconstitution with mMCP- 4 +/+ MCs, but not with mMCP-4 -/- MCs, restored blistering, MMP-9 activation, andPMNrecruitment in mMCP-4 -/- mice. mMCP-4 also degraded the hemidesmosomal transmembrane protein BP180 both in the skin and in vitro. These results demonstrate thatmMCP-4plays two different roles in the pathogenesis of experimental BP, by both activating MMP-9and by cleaving BP180, leading to injury of the hemidesmosomes and extracellular matrix of the basement membrane zone. © 2011 by The American Society for Biochemistry and Molecular Biology, Inc.
PMID: 21880713 PMCID: PMC3199483
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