Cellular interactions in fibrogenesis

Allison, A. C.; Clark, I. A.; Davies, P.

doi:10.1136/ard.36.suppl_2.8

Cited by 42 publications

(15 citation statements)

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“…Nontoxic, nonfibrogenic mineral dust caused the release of such factors to a significantly lesser extent, suggesting that the fibrosis observed with toxic mineral dusts might be mediated by macrophage-derived factors released as a consequence of cell damage and/or death (5). In confirmation of this hypothesis, experiments using implanted diffusion chambers showed that chambers containing both macrophages and fibrogenic silica caused impressive peritoneal fibrosis, whereas chambers containing macrophages or silica alone caused relatively little fibrogenic reaction (6).…”

Section: Introductionsupporting

confidence: 65%

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Silica-stimulated monocytes release fibroblast proliferation factors identical to interleukin 1. A potential role for interleukin 1 in the pathogenesis of silicosis.

Schmidt¹,

Oliver²,

Lepe-Zuniga³

et al. 1984

J. Clin. Invest.

246

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Abstract. Previous study strongly suggests that silicotic fibrosis is mediated by macrophages and their soluble mediators. The biochemical properties of the mediators involved in silicotic fibrosis, however, are as yet ill defined. The current study, therefore, determined whether human monocyte-macrophages treated with fibrogenic silica dust released factors capable of activating fibroblasts as measured by an increase in fibroblast proliferation. Silica, but not nonfibrogenic diamond dust, stimulated the release of fibroblast proliferation factors.Moreover, the level offibroblast proliferation activity was comparable with the level of thymocyte proliferation (interleukin-1) activity in the same culture supernatants. The factors responsible for these seemingly diverse activities were found to behave identically when analyzed by gel filtration chromatography, size exclusion chromatography, isoelectrofocusing, ion exchange chromatography, and hydrophobic chromatography. Moreover, the response of these factors to four different proteases and heat (560C) was also identical, which shows that their comigration on various separation media could not be explained by noncovalent interaction between otherwise unrelated species. The data demonstrate that a monocytederived thymocyte proliferation factor having the molecular properties of interleukin 1 is capable of regulating fibroblast proliferation. In silicosis and other fibrotic disDr. Schmidt is an Investigator of The Arthritis Foundation. Address all correspondence to him

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Section: Introductionsupporting

confidence: 65%

“…Quartz silica (particle size < 5 Aim) was the generous gift of Dr. P. Davies (Merck Institute for Therapeutic Research, Rahway, NJ). This material was fibrogenic as previously reported (6). Diamond dusts (particle sizes < 0.5 jim and 1-2 jm) were kindly provided by…”

Section: Methodsmentioning

confidence: 93%

Silica-stimulated monocytes release fibroblast proliferation factors identical to interleukin 1. A potential role for interleukin 1 in the pathogenesis of silicosis.

Schmidt¹,

Oliver²,

Lepe-Zuniga³

et al. 1984

J. Clin. Invest.

246

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“…Although the processes by which inflammation produces fibrosis are not fully understood, it appears that products of immune responses acting directly, or indirectly, on the fibroblasts stimulate collagen synthesis (Allison et al, 1977). In view of this, the action of dextran sulphate and heat-aggregated IgG on collagen synthesis is both striking and interesting.…”

Section: Discussionmentioning

confidence: 99%

The relationship between collagen and C1q biosynthesis in cultured human fibroblasts

Fleming¹,

McGee²

1982

Biochemical Journal

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The relationship between collagen and C lq biosynthesis has been investigated in cultured human fibroblasts. This was done by measuring the effects of variation in cell density, inhibition of prolyl hydroxylase and complexing of C lq on synthesis and/or secretion of both proteins. It was found that synthesis and secretion of both proteins were not co-ordinate, and that therefore regulation of expression of both proteins is probably not linked. However complexing of Clq did result in marked stimulation in collagen synthesis, suggesting that the fibrosis which follows inflammation may result from binding of C lq to the immune complexes formed in the inflammatory process.

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“…As will be reported subsequently (10), the presence of heat-inactivated fetal calf serum in this system not only reduces cytotoxicity of some fibers but also reduces the effects of mineral fibers on colony morphology, giant cell formation, and number of multinucleated cells per colony being manifested. The cytotoxic effects of mineral dusts on fibroblast cell cultures differ from those seen in macrophage cultures in that silica, a relatively weak carcinogen but relatively strong inducer of fibrosis, had very little cytotoxicity in fibroblast cell cultures but was a strong cytotoxic agent in macrophage cultures (8,11). Additionally, mineral fibers have been reported to induce giant cell formation (8), polyploidy in Chinese hamster ovary cell cultures (12), chromosomal aberrations in Syrian hamster embryo cells (12), and gene mutation at the hypoxanthine-guanine phosphoribosyl transferase loci in Chinese hamster lung cells (13).…”

Section: Biological Effectsmentioning

confidence: 99%

Elemental modifications and polycyclic aromatic hydrocarbon metabolism in human fibroblasts

Hart¹,

Daniel²,

Kindig³

et al. 1980

Environ Health Perspect

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Mineral fibers and particulates represent one of the best documented, economically important, and ubiquitously occurring categories of human carcinogens. Yet, while a wealth of information exists concerning the mechanism of action of physical, chemical, and viral carcinogens, virtually nothing is known relative to the mechanism of action of this economically important class of carcinogenic compounds known as mineral fibers and particulates. While the length and diameter of various forms of asbestos have been associated with both cellular toxicity in vitro and tumor occurrence in vivo, nothing is known about whether or not these same physical properties are responsible for the purported synergistic interaction between cigarette smoking and asbestos exposure relative to the induction of bronchogenic carcinoma. Thus, while the risk of bronchogenic carcinoma for nonsmokers exposed to asbestos appears to be only slightly greater than that for unexposed nonsmoking populations, the risk of occurrence of this same tumor in asbestos workers who also smoke is approximately 100-fold greater than in nonsmoking asbestos workers. The risk of bronchogenic carcinoma is increased approximately 8-fold in asbestos workers who smoke over nonexposed smokers. Since it is clear that cigarette smoke contains over 150 polycyclic aromatic hydrocarbons, some of which are known animal carcinogens, and since other laboratories have reported that metals associated with asbestos redirect the metabolism of these agents, it was of interest to us to investigate the effects of mineral fibers on the metabolism and biochemistry of polycyclic aromatic hydrocarbons.

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Cellular interactions in fibrogenesis

Cited by 42 publications

References 0 publications

Silica-stimulated monocytes release fibroblast proliferation factors identical to interleukin 1. A potential role for interleukin 1 in the pathogenesis of silicosis.

Silica-stimulated monocytes release fibroblast proliferation factors identical to interleukin 1. A potential role for interleukin 1 in the pathogenesis of silicosis.

The relationship between collagen and C1q biosynthesis in cultured human fibroblasts

Elemental modifications and polycyclic aromatic hydrocarbon metabolism in human fibroblasts

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