Immunohistochemical localization of transforming growth factor-β1 in Kaposi's sarcoma

Williams, A. Olufemi; Ward, Jerrold M.; Li, John F; Jackson, Marcus; Flanders, Kathleen C.

doi:10.1016/0046-8177(95)90241-4

Cited by 14 publications

(2 citation statements)

References 37 publications

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“…Certainly, both alveolar macrophages and epithelial cells secrete proinflammatory mediators following exposure to silica (21,28,32,39). However, despite the close proximity of fibroblasts to inhaled crystalline silica particles when the epithelial layer has been denuded, the contribution of fibroblasts to silica-induced inflammation and fibrosis has not been well studied (32a).…”

mentioning

confidence: 99%

Crystalline and amorphous silica differentially regulate the cyclooxygenase-prostaglandin pathway in pulmonary fibroblasts: implications for pulmonary fibrosis

O’Reilly¹,

Phipps²,

Thatcher³

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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Inhalation of crystalline (CS) and amorphous silica (AS) results in human pulmonary inflammation. However, silicosis develops only following CS exposure, and the pathogenic mechanisms are poorly understood. This report describes the differential abilities of CS and AS to directly upregulate the early inflammatory mediator COX-2, the recently identified prostaglandin E (PGE) synthase and the downstream mediator PGE 2 in primary human lung fibroblasts. Increased cyclooxygenase (COX)-2 gene transcription and protein production were demonstrated by ribonuclease protection assay, Western blot analysis, and immunocytochemistry. In each case the ability of AS to induce COX-2 exceeded that of CS. Similarly, downstream of COX-2, production of the antifibrotic prostaglandin PGE 2 was induced in a dose-dependent fashion, but AS was significantly more potent (maximal production: CS ϭ 4,710 pg/ml and AS ϭ 7,651 pg/ml). These increases in COX-2 and PGE 2 were preceded by induction of the PGE2 synthase protein, demonstrating the potential role of this novel molecule in silica-mediated inflammation. There was specificity of induction of prostaglandins, as PGF 2␣, but not PGD2, was induced. Using specific COX-2 inhibitors, we showed increased PG production to be dependent on the COX-2 enzyme. Furthermore, stimulation of fibroblasts was particle specific, as silica but not carbon black resulted in fibroblast activation. These results demonstrate that silica can directly stimulate human lung fibroblasts to produce key inflammatory enzymes and prostaglandins. Moreover, they suggest a mechanism to explain the differing fibrogenic potential of CS and AS. The molecules COX-2, PGE synthase, and PGE 2 are identified as effectors in silicosis.

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mentioning

confidence: 99%

Crystalline and amorphous silica differentially regulate the cyclooxygenase-prostaglandin pathway in pulmonary fibroblasts: implications for pulmonary fibrosis

O’Reilly¹,

Phipps²,

Thatcher³

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…TGF-β is a well-characterized fibrogenic mediator and it has long been known that TGF-β expression is increased in silicosis. In rats, after a single intratracheal infusion of silica, TGF-β peptide was detected in fibroblasts and macrophages surrounding silicotic granuloma and fibroblasts adjacent to hyperplastic type II cells in the lungs ( Williams et al, 1993 ). The major role of TGF-β in silicosis is the promotion of ECM accumulation, EMT induction, and the inhibition of matrix degradation.…”

Section: Inflammatory Factorsmentioning

confidence: 99%

The role of inflammation in silicosis

Liu,

Sun,

Han

et al. 2024

Front. Pharmacol.

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Silicosis is a chronic illness marked by diffuse fibrosis in lung tissue resulting from continuous exposure to SiO2-rich dust in the workplace. The onset and progression of silicosis is a complicated and poorly understood pathological process involving numerous cells and molecules. However, silicosis poses a severe threat to public health in developing countries, where it is the most prevalent occupational disease. There is convincing evidence supporting that innate and adaptive immune cells, as well as their cytokines, play a significant role in the development of silicosis. In this review, we describe the roles of immune cells and cytokines in silicosis, and summarize current knowledge on several important inflammatory signaling pathways associated with the disease, aiming to provide novel targets and strategies for the treatment of silicosis-related inflammation.

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Expression of transforming growth factor-? (TGF-?) isoforms in osteosarcomas

Kloen

Gebhardt

Perez‐Atayde

et al. 1997

Cancer

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All osteosarcomas expressed TGF-beta in the cytoplasm of the tumor cells as well as in their extracellular stroma. The presence of TGF-beta in the endothelial and perivascular layers of small vessels in the tumor stroma suggests angiogenic activity of this growth factor. The expression of TGF-beta3 was correlated strongly with disease progression (P = 0.027). These data suggest that increased expression of TGF-beta isoforms, especially TGF-beta3, may play a role in osteosarcoma progression.

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Immunohistochemical localization of transforming growth factor-β1 in Kaposi's sarcoma

Cited by 14 publications

References 37 publications

Crystalline and amorphous silica differentially regulate the cyclooxygenase-prostaglandin pathway in pulmonary fibroblasts: implications for pulmonary fibrosis

Crystalline and amorphous silica differentially regulate the cyclooxygenase-prostaglandin pathway in pulmonary fibroblasts: implications for pulmonary fibrosis

The role of inflammation in silicosis

Expression of transforming growth factor-? (TGF-?) isoforms in osteosarcomas

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