Degradation of cartilage proteoglycan and collagen by synovial cells. Stimulation by macrophages under activation by phagocytosis, lymphocyte factors, bacterial products or other inflammatory stimuli

Our plain-English summary of Degradation of cartilage proteoglycan and collagen by synovial cells. Stimulation by macrophages under activation by phagocytosis, lymphocyte factors, bacterial products or other inflammatory stimuli, by C. Peeters-Joris, G. Vaes (Biochimica et Biophysica Acta, 1984).

The study

• Authors: C. Peeters-Joris, G. Vaes
• Journal: Biochimica et Biophysica Acta
• Published: 1984;804(4):474-86
• Cited by: 16 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

When cultured together with dead 35S-labelled cartilage discs or at the surface of [3H]proteoglycan/[14C]collagen-coated plates, synovial cells from either arthritic or normal rabbit joints digested both the proteoglycan and the collagen of the substrates after a lag-period of 1-2 days. These digestions were inversely related to the age (number of subculture passages) of the synovial cells and they could be modulated by serum components that were either inhibitory or stimulatory. They were dependent on a protein synthesis by the cells and were paralleled, in young cultures, by the release of collagenase and of a proteoglycan-degrading neutral proteinase. The co-culture of synovial cells with macrophages or their culture with macrophage-conditioned culture media caused a more rapid and more extensive degradation of collagen and proteoglycan due to the stimulation of the synovial cells by a nondialysable macrophage factor. The production of this synovial cell-activating 'matrix regulatory monokine' by the macrophage was enhanced by several immunological or inflammatory stimuli such as lymphocyte factors, phagocytosis, asbestos fibres, endotoxin, adjuvant muramyl dipeptide or chemotactic formyl-methionyl peptide, as well as by other membrane-active agents (phorbol myristate acetate, concanavalin A). It is presumed that these interactions are of importance in the development of cartilage destruction in rheumatoid and other chronic inflammatory arthritis.

In plain English

This laboratory study used rabbit cells, not people, and concerned arthritis rather than asbestos disease. The authors grew synovial cells (joint-lining cells) from the knees of normal rabbits and rabbits with an experimentally induced immune arthritis, alongside cartilage or plates coated with cartilage proteoglycan and collagen. After a lag of 1-2 days, cells from both normal and arthritic joints broke down both materials. This depended on the cells making protein, and the capacity faded with repeated subculture. Macrophages (immune cells), or fluid in which macrophages had been grown, made the synovial cells break down collagen and proteoglycan faster and more extensively, through a factor the macrophages released. Several stimuli increased the macrophages' release of this factor, including particles such as zymosan, lymphocyte products, bacterial products and asbestos. The asbestos was UICC chrysotile B, tested at 100, 200 or 400 micrograms per millilitre. The authors called it a potent stimulant but could not clearly confirm that the fibres were engulfed. The authors presumed these interactions matter in cartilage destruction in rheumatoid and other chronic inflammatory arthritis.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: laboratory (in vitro) cell culture experiments using rabbit cells
• Who was studied: Synovial cells from the knee joints of normal rabbits and of rabbits with an experimentally induced immune arthritis, and bone marrow-derived macrophages from male rabbits (Termonde White or New Zealand strain), in Belgium
• Exposure: UICC chrysotile B asbestos added to macrophage cultures, as one of several macrophage-activating stimuli. The others were zymosan, carbonyl iron, latex particles, lymphocyte-conditioned media, endotoxin, muramyl dipeptide, formyl-methionyl peptide, phorbol myristate acetate and concanavalin A.
• Main results:
  • After a lag of 1-2 days, synovial cells from either normal or arthritic joints degraded both proteoglycan and collagen on coated plates.
  • Degradation was suppressed by cycloheximide or by lysing the cells, which the authors took to suggest it depended on protein synthesis by the cells.
  • After the first subculture passage, with Sepharose-trypsin-treated serum added, cells from normal and arthritic rabbits were equally efficient at degrading cartilage proteoglycan and collagen.
  • After more subculture passages, synovial cells progressively lost their capacity to degrade the substrates spontaneously.
  • Co-culture with macrophages caused more rapid and more extensive collagen degradation by synovial cells. Macrophage-conditioned medium also stimulated degradation of both collagen and proteoglycan.
  • Asbestos (tested at 100, 200 or 400 micrograms per millilitre) was described as a potent stimulant of macrophage release of the synovial cell-activating factor.
  • The asbestos doses used to stimulate macrophages were 100, 200 or 400 (micrograms per millilitre, per the figure legend).
  • Phagocytosis of zymosan was particularly active in enhancing release of the factor. Latex beads were less efficient and gave more variable results.
  • Endotoxin, the adjuvant peptide and the chemotactic peptide were also good activators of production of the factor.
• The authors' conclusion: The authors presumed that these macrophage-synovial cell interactions are of importance in the development of cartilage destruction in rheumatoid and other chronic inflammatory arthritis.
• Limitations the authors state:
  • Phagocytosis of asbestos by the macrophages could not be clearly established by microscopic examination.
  • The identity of the synovial cell-activating factor with the fibroblast-activating monokine remains to be proven on purified material.
  • Normal and arthritic cells could not be compared in primocultures because too few cells were obtained from normal synovium.
  • A direct effect of lymphocyte factors on synovial cells could not be excluded.

Topics

Medical terms in this study, explained in our Lexicon: Collagen, Macrophage, Phagocytosis.

Related studies

• Macrophage stimulation and the inflammatory response to asbestos — J.A. Hamilton (1980)
• Proteoglycans in human malignant mesothelioma. Stimulation of their synthesis induced by epidermal, insulin and platelet-derived growth factors involves receptors with tyrosine kinase activity — A. Syrokou, G.N. Tzanakakis, et al. (1999)
• The collagenous nature of amianthoid degeneration of human costal cartilage — A.J. Hough, F.C. Mottram, et al. (1973)
• Differences between particulate and peptide stimuli on activation of oxidant production in alveolar macrophages — G.E. Hatch, A. Spock, et al. (1980)
• The selective release of lysosomal acid hydrolases from mouse peritoneal macrophages by stimuli of chronic inflammation — H.U. Schorlemmer, P. Davies, et al. (1977)
• Effect of insulin and epidermal growth factors on the synthesis of glycosaminoglycans/proteoglycans in cultured human malignant mesothelioma cells of different phenotypic morphology — G.N. Tzanakakis, N.K. Karamanos, et al. (1996)

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