Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Publication alerts by email
  • Advertising
  • Job board
  • Contact
  • Clinical Research and Public Health
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Video Abstracts
  • Reviews
    • View all reviews ...
    • Complement Biology and Therapeutics (May 2025)
    • Evolving insights into MASLD and MASH pathogenesis and treatment (Apr 2025)
    • Microbiome in Health and Disease (Feb 2025)
    • Substance Use Disorders (Oct 2024)
    • Clonal Hematopoiesis (Oct 2024)
    • Sex Differences in Medicine (Sep 2024)
    • Vascular Malformations (Apr 2024)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Clinical Research and Public Health
    • Research Letters
    • Letters to the Editor
    • Editorials
    • Commentaries
    • Editor's notes
    • Reviews
    • Viewpoints
    • 100th anniversary
    • Top read articles

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Video Abstracts
  • In-Press Preview
  • Clinical Research and Public Health
  • Research Letters
  • Letters to the Editor
  • Editorials
  • Commentaries
  • Editor's notes
  • Reviews
  • Viewpoints
  • 100th anniversary
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Publication alerts by email
  • Advertising
  • Job board
  • Contact
Thrombospondins as matricellular modulators of cell function
Paul Bornstein
Paul Bornstein
Published April 15, 2001
Citation Information: J Clin Invest. 2001;107(8):929-934. https://doi.org/10.1172/JCI12749.
View: Text | PDF
Perspective

Thrombospondins as matricellular modulators of cell function

  • Text
  • PDF
Abstract

Authors

Paul Bornstein

×

Figure 1

Options: View larger image (or click on image) Download as PowerPoint
A proposed scheme to account for the modulation of pericellular MMP2 lev...
A proposed scheme to account for the modulation of pericellular MMP2 levels by TSP2. TSP2, ProMMP2, and TIMP2 are secreted into the pericellular environment, either individually or together, by fusion of secretory vesicles with the plasma membrane (double line). As shown on the right side of the figure, ProMMP2, in a complex with TIMP2, can be activated by membrane-bound MT1-MMP to form active MMP2, which is capable of reducing adhesion by cleaving matrix-bound proteins and proteoglycans, and possibly adhesion receptors. When TSP2 is present, a competing pathway clears ProMMP2 from the cell surface. Thus, as shown on the left, TSP2 can bind either ProMMP2 or active MMP2. This complex is then bound by the LRP receptor, endocytosed, and directed to lysosomes for degradation. Since the binding of (Pro)MMP2 to TIMP2 is of considerably higher affinity than that to TSP2, it is possible that a trimolecular complex that includes TIMP2 is endocytosed by LRP. However, TSP2 could still compete effectively with TIMP2 for binding to ProMMP2 or MMP2 by mass action, if the [TSP2] >> [(Pro)MMP2] and if the TSP2/(Pro)MMP2 complex were constantly removed by endocytosis. Alternatively, the TSP2/(Pro)MMP2 complex could be bound to the matrix, thus reducing the bioavailability of the protease.

Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts