Literature DB >> 15472125

Granzyme B induces smooth muscle cell apoptosis in the absence of perforin: involvement of extracellular matrix degradation.

Jonathan C Choy1, Vivian H Y Hung, Arwen L Hunter, Paul K Cheung, Bruce Motyka, Ing Swie Goping, Tracy Sawchuk, R Chris Bleackley, Thomas J Podor, Bruce M McManus, David J Granville.   

Abstract

OBJECTIVE: T cell-induced cytotoxicity, of which granzyme B is a key mediator, is believed to contribute to the pathogenesis of inflammatory vascular diseases. In this report, we investigate the mechanism of granzyme B-induced smooth muscle cell (SMC) death. METHODS AND
RESULTS: The addition of purified granzyme B alone to cultured SMCs caused a significant reduction in cell viability. Chromatin condensation, phosphatidylserine externalization, and membrane blebbing were observed, indicating that the mechanism of granzyme B-induced SMC death was through apoptosis. Activated splenocytes from perforin-knockout mice induced SMC death through a granzyme B-mediated pathway. Inhibition of the proteolytic activities of caspases and granzyme B prevented granzyme B-induced SMC death, whereas attenuation of granzyme B internalization with mannose-6-phosphate (M6P) did not. Further, granzyme B induced the cleavage of several SMC extracellular proteins, including fibronectin, and reduced focal adhesion kinase phosphorylation.
CONCLUSIONS: These results indicate that granzyme B can induce apoptosis of SMCs in the absence of perforin by cleaving extracellular proteins, such as fibronectin.

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Year:  2004        PMID: 15472125     DOI: 10.1161/01.ATV.0000147162.51930.b7

Source DB:  PubMed          Journal:  Arterioscler Thromb Vasc Biol        ISSN: 1079-5642            Impact factor:   8.311


  30 in total

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