MMPs and other matrix-degrading metalloproteinases in neurological disease

P. E. Gottschall, K. Conant

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

The metzincin superfamily of metalloproteinases includes the most well-studied matrix metalloproteinases (MMPs), the ADAMs (a disintegrin and metalloproteinase), and the ADAMTSs (ADAM with thrombospondin repeats) families of extracellular matrix (ECM)-degrading enzymes. These proteases are mostly secreted with important exceptions for the transmembrane sheddases and can degrade all protein components of the ECM. In addition to ECM proteins, secreted and cell-surface proteins including growth factors, cytokines, and chemokines may be cleaved by the MMPs. These proteases alter the composition and structural organization of the ECM; and importantly, cleavage affects intracellular signaling induced by binding of matrix molecules to cell-surface receptors. A body of data has been generated on the expression of these proteases in neurological disease, which is summarized here. In addition, the role of individual MMPs in particular animal models of disease has been investigated using genetically targeted mutant mice. In general, these results have suggested a detrimental role for the MMPs that relates to the induction of their expression in response to injury or disease.

Original languageEnglish (US)
Title of host publicationHandbook of Neurochemistry and Molecular Neurobiology
Subtitle of host publicationNeural Protein Metabolism and Function
PublisherSpringer US
Pages565-590
Number of pages26
ISBN (Print)9780387303468
DOIs
StatePublished - Dec 1 2007

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)

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    Gottschall, P. E., & Conant, K. (2007). MMPs and other matrix-degrading metalloproteinases in neurological disease. In Handbook of Neurochemistry and Molecular Neurobiology: Neural Protein Metabolism and Function (pp. 565-590). Springer US. https://doi.org/10.1007/978-0-387-30379-6_19