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Elastases and elastin degradation

Z Werb, M J Banda, J H McKerrow

    The Journal of Investigative Dermatology
    |July 1, 1982
    PubMed
    Summary
    This summary is machine-generated.

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    Elastin degradation, driven by various enzymes, contributes to disease and is linked to bacterial and venom pathogenicity. Imbalances in proteinase inhibitors like alpha 1-proteinase inhibitor can lead to elastin destruction.

    Area of Science:

    • Biochemistry
    • Molecular Biology
    • Pathology

    Background:

    • Mature elastin fibers exhibit slow metabolic turnover in adult animals.
    • While normal elastin degradation is minimal, increased breakdown and fragmentation of elastic fibers are implicated in disease processes.
    • Elastinolytic enzymes are present in microorganisms, snake venoms, and mammalian cells, including pancreas, polymorphonuclear leukocytes, and macrophages.

    Purpose of the Study:

    • To review the role of elastinolytic enzymes in health and disease.
    • To understand the diverse nature and specificity of elastinolytic enzymes.
    • To highlight the significance of elastin degradation in pathogenicity and disease induction, such as experimental pulmonary emphysema.

    Main Methods:

    • Review of existing literature on elastinolytic enzymes and their substrates.

    Related Experiment Videos

  • Analysis of the classification and catalytic activities of various elastases.
  • Examination of the role of elastin degradation in different biological contexts, including microbial infections, venom activity, and mammalian cell interactions.

    • Main Results:

    • Elastinolytic enzymes encompass all four proteinase classes (aspartic, cysteine, serine, metallo) with varied specificities.
    • These enzymes exhibit catalytic activity against non-elastin protein and peptide substrates.
    • Elastase activity is a virulence factor in pathogens like Pseudomonas and fungi, and in rattlesnake venom.
    • Only elastinolytic enzymes can induce experimental pulmonary emphysema.
    • Macrophage and trophoblast-mediated elastin degradation is localized pericellularly.
    • Mammalian elastase-mediated elastin destruction often results from an imbalanced inhibitor-proteinase ratio, primarily involving alpha 1-proteinase inhibitor and alpha 2-macroglobulin.

    Conclusions:

    • Elastin degradation is a critical factor in various disease processes and pathogenicity.
    • The balance between elastases and their inhibitors (e.g., alpha 1-proteinase inhibitor, alpha 2-macroglobulin) is crucial for regulating elastin integrity.
    • Understanding elastinolytic enzymes offers insights into disease mechanisms and potential therapeutic targets.