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Dual targets for mouse mast cell protease-4 in mediating tissue damage in experimental bullous pemphigoid

Lan Lin; Eric Bankaitis; Lisa Heimbach; Ning Li; Magnus Abrink; Gunnar Pejler; Lijia An; Luis A. Diaz; Zena Werb; Zhi Liu (Profiled Authors: Luis A Diaz; Zhi Liu; Ning Li)

Journal of Biological Chemistry. 2011;286(43):37358-37367.

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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