Release of collagen type IV degrading activity from C6 astrocytoma cells and cell density

1996 ◽  
Vol 84 (6) ◽  
pp. 1013-1019 ◽  
Author(s):  
Masashi Tamaki ◽  
Warren McDonald ◽  
Rolando F. Del Maestro
Keyword(s):  
Cell Density ◽  
Collagen Type ◽  
Cell Communication ◽  
Collagen Type Iv ◽  
Major Protein ◽  
Content Type ◽  
Type Iv ◽  
Astrocytoma Cells ◽  
C6 Astrocytoma

✓ Type IV collagen is a major protein component of the vascular basement membrane and its degradation is crucial to the initiation of tumor-associated angiogenesis. The authors have investigated the influence of cell density on the release of collagen type IV degrading activity by C6 astrocytoma cells in monolayer culture. The release of collagen type IV degrading activity was assessed biochemically, immunocytochemically, and by Western blot analysis. The results demonstrate that increasing plating density and increasing cell density are associated with decreased collagen type IV degrading activity released per tumor cell. These findings indicate the existence of regulatory mechanisms dependent on cell—cell communication, which modulate release of collagen type IV degrading activity. The extrapolation of these results to the in vivo tumor microenvironment would suggest that individual and/or small groups of invading tumor cells, distant from the main tumor mass, would release substantial collagen type IV degrading activity, which may be crucial to their continued invasion and to angiogenesis.

Degradation of collagen type IV by C6 astrocytoma cells

1995 ◽  
Vol 24 (1) ◽  
pp. 75-81 ◽  
Author(s):  
Rolando F. Del Maestro ◽  
Indrasen S. Vaithilingam ◽  
Warren McDonald
Keyword(s):  
Collagen Type ◽  
Collagen Type Iv ◽  
Type Iv ◽  
Astrocytoma Cells ◽  
C6 Astrocytoma

Serum proteolytic activity during the growth of C6 astrocytoma

1992 ◽  
Vol 77 (4) ◽  
pp. 595-600 ◽  
Author(s):  
Indrasen S. Vaithilingam ◽  
Warren McDonald ◽  
Noel K. Brown ◽  
Eric Stroude ◽  
Robert A. Cook ◽  
...  
Keyword(s):  
Proteolytic Activity ◽  
Type Iv Collagen ◽  
Collagenase Activity ◽  
Type Iv Collagenase ◽  
Content Type ◽  
Type Iv ◽  
Astrocytoma Cells ◽  
Vessel Remodeling ◽  
C6 Astrocytoma ◽  
Fine Print

✓ Tumor growth is dependent on the ability of neoplastic cells to induce angiogenesis. Blood-vessel remodeling requires the reconstruction of the nonfibrous proteins and type IV collagen components of the basement membrane. This study has assessed the influence of the growth of C6 astrocytoma cells in the rat spheroid implantation model on serum general protease and type IV collagenase activity. The results demonstrate that general protease activity increased in serum, reaching maximum values on Day 6 and Day 13 following spheroid implantation, and that type IV collagenase activity increased in serum, obtaining maximum values on Day 8 and Day 15. The measurement of serum proteolytic activity may be of value in the detection of recurrent tumors.

scholarly journals First Analysis of a Bacterial Collagen-Binding Protein with Collagen Toolkits: Promiscuous Binding of YadA to Collagens May Explain How YadA Interferes with Host Processes

2010 ◽  
Vol 78 (7) ◽  
pp. 3226-3236 ◽  
Author(s):  
Jack C. Leo ◽  
Heli Elovaara ◽  
Dominique Bihan ◽  
Nicholas Pugh ◽  
Sami K. Kilpinen ◽  
...  
Keyword(s):  
Pathogenic Bacteria ◽  
Binding Proteins ◽  
Collagen Type ◽  
Collagen Type Iv ◽  
Collagen Binding ◽  
Type Iv ◽  
Helical Peptide ◽  
Binding Peptides ◽  
Binding Determinants

ABSTRACT The Yersinia adhesin YadA mediates the adhesion of the human enteropathogen Yersinia enterocolitica to collagens and other components of the extracellular matrix. Though YadA has been proposed to bind to a specific site in collagens, the exact binding determinants for YadA in native collagen have not previously been elucidated. We investigated the binding of YadA to collagen Toolkits, which are libraries of triple-helical peptides spanning the sequences of type II and III human collagens. YadA bound to many of them, in particular to peptides rich in hydroxyproline but with few charged residues. We were able to block the binding of YadA to collagen type IV with the triple-helical peptide (Pro-Hyp-Gly)10, suggesting that the same site in YadA binds to triple-helical regions in network-forming collagens as well. We showed that a single Gly-Pro-Hyp triplet in a triple-helical peptide was sufficient to support YadA binding, but more than six triplets were required to form a tight YadA binding site. This is significantly longer than the case for eukaryotic collagen-binding proteins. YadA-expressing bacteria bound promiscuously to Toolkit peptides. Promiscuous binding could be advantageous for pathogenicity in Y. enterocolitica and, indeed, for other pathogenic bacteria. Many of the tightly binding peptides are also targets for eukaryotic collagen-binding proteins, and YadA was able to inhibit the interaction between selected Toolkit peptides and platelets. This leads to the intriguing possibility that YadA may interfere in vivo with host processes mediated by endogenous collagen-binding proteins.

Implantation of C6 astrocytoma spheroid into collagen type I gels: invasive, proliferative, and enzymatic characterizations

1997 ◽  
Vol 87 (4) ◽  
pp. 602-609 ◽  
Author(s):  
Masashi Tamaki ◽  
Warren McDonald ◽  
Verena R. Amberger ◽  
Emi Moore ◽  
Rolando F. Del Maestro
Keyword(s):  
Collagen Type ◽  
Single Cells ◽  
Malignant Gliomas ◽  
Collagen Type I ◽  
Collagen Type Iv ◽  
Type I ◽  
Three Dimensional Model ◽  
Content Type ◽  
C6 Astrocytoma ◽  
Fine Print

✓ A three-dimensional model has been developed in which C6 astrocytoma spheroids of defined sizes are embedded into collagen type I gels. The authors have monitored cell invasive behavior; obtained quantitative data on cell invasion, proliferation, and enzymatic activity; assessed cell—cell interactions by altering the spheroid size used; and studied cell—matrix interactions by modifying the matrix components. Their results show that C6 astrocytoma cells detach from the spheroid surface and invade the gel as single cells by means of a system that appears to be dependent on metalloprotease function. These invasive cells have a low proliferative index. Larger spheroids with central hypoxic microregions possess cells that invade the gel at faster rates; this could be correlated with the release of increased collagen type I degrading activity. Extracellular matrix proteins, such as laminin, fibronectin, and collagen type IV have no significant influence on invasive activity, whereas hyaluronic acid decreases and human central nervous system myelin increases invasion. New strategies directed at the treatment of malignant gliomas must take into account the subpopulation of malignant cells located long distances from the major tumor mass. The spheroid invasion model may provide specific insights into the behavior of these invasive cells.

Ultrastructural triple localization of laminin-1, nidogen-1, and collagen type IV helps elucidate basement membrane structure in vivo

1999 ◽  
Vol 254 (3) ◽  
pp. 382-388 ◽  
Author(s):  
Nicolai Miosge ◽  
Steffen Heinemann ◽  
Andreas Leissling ◽  
Christina Klenczar ◽  
Rainer Herken
Keyword(s):  
Basement Membrane ◽  
Membrane Structure ◽  
Collagen Type ◽  
Collagen Type Iv ◽  
Type Iv ◽  
Nidogen 1 ◽  
Laminin 1

scholarly journals Proteolytic exposure of a cryptic site within collagen type IV is required for angiogenesis and tumor growth in vivo

2001 ◽  
Vol 154 (5) ◽  
pp. 1069-1080 ◽  
Author(s):  
Jingsong Xu ◽  
Dorothy Rodriguez ◽  
Eric Petitclerc ◽  
Jenny J. Kim ◽  
Masanori Hangai ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Endothelial Cell ◽  
Tumor Growth ◽  
Collagen Type ◽  
Helical Structure ◽  
Regulatory Elements ◽  
Collagen Type Iv ◽  
Type Iv ◽  
Triple Helical Structure

Evidence is provided that proteolytic cleavage of collagen type IV results in the exposure of a functionally important cryptic site hidden within its triple helical structure. Exposure of this cryptic site was associated with angiogenic, but not quiescent, blood vessels and was required for angiogenesis in vivo. Exposure of the HUIV26 epitope was associated with a loss of α1β1 integrin binding and the gain of αvβ3 binding. A monoclonal antibody (HUIV26) directed to this site disrupts integrin-dependent endothelial cell interactions and potently inhibits angiogenesis and tumor growth. Together, these studies suggest a novel mechanism by which proteolysis contributes to angiogenesis by exposing hidden regulatory elements within matrix-immobilized collagen type IV.

scholarly journals Evaluation of the Trimeric Autotransporter Ata as a Vaccine Candidate against Acinetobacter baumannii Infections

2012 ◽  
Vol 80 (10) ◽  
pp. 3381-3388 ◽  
Author(s):  
Leticia V. Bentancor ◽  
Abhisek Routray ◽  
Cagla Bozkurt-Guzel ◽  
Ana Camacho-Peiro ◽  
Gerald B. Pier ◽  
...  
Keyword(s):  
Acinetobacter Baumannii ◽  
Collagen Type ◽  
Basal Membrane ◽  
Multidrug Resistant ◽  
Collagen Type Iv ◽  
Polymorphonuclear Cells ◽  
Content Type ◽  
Type Iv ◽  
Protective Antibodies ◽  
Immunocompromised Mice

ABSTRACTAcinetobacter baumanniiis a multidrug-resistant (MDR) nosocomial pathogen for which immunotherapeutic alternatives are needed. We previously identified a surface autotransporter ofA. baumannii, Ata, that bound to various extracellular matrix/basal membrane proteins and was required for full virulence, biofilm formation, and the adhesion ofA. baumanniito collagen type IV. We show here that Ata binding to collagen type IV was inhibited by antibodies to Ata. In addition, in the presence of complement and polymorphonuclear cells (PMNs), antibodies to Ata were highly opsonic againstA. baumanniiATCC 17978 and showed low to moderate killing activity against four heterologousA. baumanniistrains, whereas in the absence of PMNs, antibody to Ata efficiently promoted complement-dependent bactericidal killing of all of the testedA. baumanniiisolates. Using a pneumonia model of infection in both immunocompetent and immunocompromised mice, we found that, compared to normal rabbit sera, antisera to Ata significantly reduced the levels ofA. baumanniiATCC 17978 and two MDR strains in the lungs of infected mice. The ability of Ata to engender anti-adhesive, bactericidal, opsonophagocytic, and protective antibodies validates its potential use as an antigenic target against MDRA. baumanniiinfections.

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