Partial characterization of the macrophage factor that stimulates fibroblasts to produce collagenase and to degrade collagen

Huybrechts-Godin, G; Peeters-Joris, Chantal; Vaes, Gilbert

doi:10.1016/0167-4889(85)90109-0

Cited by 26 publications

(5 citation statements)

References 7 publications

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“…Later investigations focused on the identity of the factors responsible for the induction of fibroblast collagenase synthesis (Huybrechts-Godin et al, 1985). On the basis of similarities in the physical characteristics of the purified factor, several independent laboratories concluded that the active material is IL-Iß (Ito et al, 1988;Unemori et al, 1994).…”

Section: Regulation Of Fibroblast Metalloproteinase Secretion By Macrmentioning

confidence: 99%

Macrophage Involvement in Wound Repair, Remodeling, and Fibrosis

Riches

1988

The Molecular and Cellular Biology of Wound Repair

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Section: Regulation Of Fibroblast Metalloproteinase Secretion By Macrmentioning

confidence: 99%

Macrophage Involvement in Wound Repair, Remodeling, and Fibrosis

Riches

1988

The Molecular and Cellular Biology of Wound Repair

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“…Although a cervical collagenase has been isolated [13] it had so far not been possible to directly demonstrate elevated collagenase activity in the cervix during labour. There was, however, circumstantial evidence since elevated collagenase activities had been found in samples obtained immediately post partum [3,5,8,12,13,18,22,30,37,38].…”

Section: Discussionmentioning

confidence: 93%

Collagenase activity in the cervix of non-pregnant and pregnant women

Osmers

Rath

Adelmann-Grill

et al. 1990

Arch Gynecol Obstet

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Cervical biopsies were obtained from non pregnant patients and from pregnant at various stages of gestation and during labour. The tissues were extract with a Ca(++)-containing buffer, and collagenase activity was determined in these extracts using a solid phase assay in which triple helical 125I-labelled collagen was cleaved. Collagenase was detected in all samples but significantly elevated activity was only present in labour at 6-8 cm cervical dilatation. This provides direct evidence for the crucial role of specific collagen degradation during cervical ripening and dilatation.

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“…Macrophages and fibroblasts not only combine in fibrogenesis but individually are able to reverse the process by production of collagenases. Macrophage populations from various sources differed widely in their capacity to degrade collagen and proteoglycans, but fibroblasts possessed greater collagen degrading ability and could be stimulated to do so by a cytokine secreted by macrophages (301,302). Moreover, human alveolar macrophages proved capable of producing in culture not only a procollagenase but also a collagenase inhibitor, both of which were indistnguishable from analogous products ofhuman fibroblasts (303,304).. Degradation of procollagen probably occurs intracellularly and soon after synthesis, but degradation of extracellular collagen, that is where cross links are established, is a slower process to avoid destabilization of structure (305).…”

Section: Connective Tissue Destructionmentioning

confidence: 99%

Minerals, fibrosis, and the lung.

Heppleston

1991

Environ Health Perspect

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Determinants of pulmonary fibrosis induced by inhaled mineral dusts include quantity retained, particle size, and surface area, together with their physical form and the reactive surface groups presented to alveolar cells. The outstanding problem is to ascertain how these factors exert their deleterious effects. Both compact and fibrous minerals inflict membrane damage, for which chemical mechanisms still leave uncertainty. A major weakness of cytotoxicity studies, even when lipid peroxidation and reactive oxygen species are considered, lies in tacitly assuming that membrane damage suffices to account for fibrogenesis, whereas the parallel occurrence of such manifestations does not necessarily imply causation. The two-phase procedure established that particles, both compact and fibrous, induce release of a macrophage factor that provokes fibroblasts into collagen synthesis. The amino acid composition of the macrophage fibrogenic factor was characterized and its intracellular action explained. Fibrous particles introduce complexities respecting type, durability, and dimensions. Asbestotic fibrosis is believed to depend on long fibers, but scrutiny of the evidence from experimental and human sources reveals that a role for short fibers needs to be entertained. Using the two-phase system, short fibers proved fibrogenic. Other mechanisms, agonistic and antagonistic, may participate. Growth factors may affect the fibroblast population and collagen production, with cytokines such as interleukin-1 and tumor necrosis factor exerting control. Immune involvement is best regarded as an epiphenomenon. Downregulation of fibrogenesis may follow collagenase release from macrophages and fibroblasts, while augmented type II cell secretion of lipid can interfere with the macrophage-particle reaction.

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Partial characterization of the macrophage factor that stimulates fibroblasts to produce collagenase and to degrade collagen

Cited by 26 publications

References 7 publications

Macrophage Involvement in Wound Repair, Remodeling, and Fibrosis

Macrophage Involvement in Wound Repair, Remodeling, and Fibrosis

Collagenase activity in the cervix of non-pregnant and pregnant women

Minerals, fibrosis, and the lung.

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