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Titolo:
Silica and its antagonistic effects on transforming growth factor-beta in lung fibroblast extracellular matrix production
Autore:
Baroni, T; Bodo, M; DAlessandro, A; Conte, C; Calvitti, M; Muzi, G; Lumare, A; Bellocchio, S; Abbritti, G;
Indirizzi:
Univ Perugia, Sez Istol, Fac Med, I-06126 Perugia, Italy Univ Perugia Perugia Italy I-06126 stol, Fac Med, I-06126 Perugia, Italy Univ Perugia, Occupat Med & Toxicol Div, Fac Med, I-06126 Perugia, Italy Univ Perugia Perugia Italy I-06126 Div, Fac Med, I-06126 Perugia, Italy
Titolo Testata:
JOURNAL OF INVESTIGATIVE MEDICINE
fascicolo: 2, volume: 49, anno: 2001,
pagine: 146 - 156
SICI:
1081-5589(200103)49:2<146:SAIAEO>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED PULMONARY FIBROSIS; FIBROTIC HAMSTER LUNGS; MESSENGER-RNA; IN-VITRO; CELLS; INTERLEUKIN-1; EXPRESSION; GLYCOSAMINOGLYCANS; INFLAMMATION; MACROPHAGES;
Keywords:
lung fibroblasts; silica; extracellular matrix; cytokines; growth factors;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Bodo, M Univ Perugia, Sez Istol, Fac Med, Via del Giochetto, I-06126 Perugia, Italy Univ Perugia Via del Giochetto Perugia Italy I-06126 rugia, Italy
Citazione:
T. Baroni et al., "Silica and its antagonistic effects on transforming growth factor-beta in lung fibroblast extracellular matrix production", J INVES MED, 49(2), 2001, pp. 146-156

Abstract

Background: Silicosis, a pneumoconiosis marked by interstitial pulmonary fibrosis, is caused by inhalation of free crystalline silica particles. Whensilica particles are injected into the lower lung, they are translocated across the epithelium into the interstitial space, where macrophage-derived growth factors affect lung fibroblast proliferation and collagen deposition, We hypothesized that silica may act directly on pulmonary fibroblasts modifying extracellular matrix (ECM) synthesis and that the effects of silica may be mediated by transforming growth factor-beta (TGF beta) overproduction. Methods: To test this hypothesis, we studied a human lung fibroblast cell line (WI-1003) exposed to silica in vitro, We investigated cell morphology by electron microscopic procedure, cell growth, collagen production, and glycosaminoglycans (GAG) composition by radiolabeled precursors. Cytokine andgrowth factor synthesis were evaluated by specific enzyme-linked immunoadsorbent assay kits and Northern blotting analysis,Results: Pulmonary fibroblasts internalized silica particles without detectable cell damage. Silica directly stimulated collagen synthesis and decreased the amount of H-3-glucosamine-labeled GAG. Silica-treated fibroblasts secreted less TGF beta than untreated controls, antagonized the stimulatory effect of TGF beta on ECM synthesis, and reversed TGF beta -induced inhibition of cell proliferation. Northern blotting analysis showed increased interleukin-1 alpha (IL-1 alpha) mRNA after silica treatment. IL-la! had no influence on collagen synthesis but increased the number of WI-1003 fibroblasts. Conclusions: These results support our hypothesis that lung fibroblasts are direct silica targets. However, contradicting our hypothesis, silica antagonized TGF beta activities through a TGF beta downregulation and an IL-1 alpha upregulation, The complex pattern of TGF beta and IL-1 alpha regulation in pulmonary fibroblasts is imbalanced by silica exposure and might play a key role in silica-mediated pulmonary fibrosis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/05/20 alle ore 13:23:07