Thrombin is present in the lungs of patients with primary extremity osteosarcoma and pulmonary metastases.

Osteosarcoma is a rare cancer, which metastasizes to the lung in up to 80% of cases. Thrombin is involved in metastasis and is present in the lungs of patients with pulmonary metastases (PM). To identify its role in PM and osteosarcoma, we measured thrombin levels in the bronchoalveolar lavage fluid (BALF) of 15 patients.

Cyclooxygenase-2 deficiency results in a loss of the anti-proliferative response to transforming growth factor-beta in human fibrotic lung fibroblasts and promotes bleomycin-induced pulmonary fibrosis in mice.

Prostaglandin E(2) (PGE(2)) inhibits fibroblast proliferation and collagen production. Its synthesis by fibroblasts is induced by profibrotic mediators including transforming growth factor (TGF)-beta(1). However, in patients with pulmonary fibrosis, PGE(2) levels are decreased.

Diverse cellular TGF-beta 1 and TGF-beta 3 gene expression in normal human and murine lung.

A role for transforming growth factor-beta 1, (TGF-beta 1) has been proposed in lung development and in the pathogenesis of pulmonary disease. However, previous studies have not delineated the cells expressing TGF-beta 1 in normal adult lung, nor compared its gene expression with that of other TGF-beta isoforms. We used digoxigenin-labelled riboprobes to localize TGF-beta 1 and TGF-beta 3 gene expression in normal adult human and mouse lung.

Maximal PDGF-induced lung fibroblast chemotaxis requires PDGF receptor-alpha.

Alteration of the platelet-derived growth factor (PDGF) receptor system could be important in enhancing the mitogenic and chemotactic potential of lung fibroblasts during pulmonary fibrogenesis. We previously reported that interleukin-1 beta (IL-1 beta) upregulates the PDGF receptor-alpha (PDGFR-alpha) gene, and in this study we sought to establish the importance of the PDGFR-alpha relative to the PDGFR-beta in mediating a chemotactic response to PDGF-AA, -AB, and -BB. Pretreatment of fibroblasts for 24 h with IL-1 beta increased chemotaxis to all three PDGF isoforms.

Role of thrombin in pulmonary fibrosis.

Pulmonary fibrosis commonly develops in systemic sclerosis. We assessed the role of thrombin in promoting fibroblast proliferation in the lungs in this disorder. Bronchoalveolar lavage fluid (BALF) thrombin concentrations were higher in ten patients with systemic sclerosis than in 12 healthy controls (14.

Platelet-derived growth factor (PDGF)-AA, -AB, and -BB induce differential chemotaxis of early-passage rat lung fibroblasts in vitro.

Platelet-derived growth factor (PDGF) isoforms are chemoattractants and mitogens for cells of mesenchymal origin that could be important mediators of pulmonary fibrogenesis. We have previously reported that particle-activated alveolar macrophages secrete homologues of PDGF that are composed of all three PDGF isoforms (PDGF-AA, -AB, and -BB). This mixture of macrophage-derived PDGF, once dissociated from the PDGF-alpha-macroglobulin complex, induces chemotaxis of rat lung fibroblasts (RLF) in the nanomolar range.

Early-passage rat lung fibroblasts do not migrate in vitro to transforming growth factor-beta.

Lung fibrosis has been postulated to be mediated by the production of macrophage-derived growth factors that are both mitogenic and chemotactic for fibroblasts. In vitro studies from our laboratory demonstrated that alveolar and interstitial macrophages treated with iron and asbestos release platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-beta) into the media. This conditioned media was capable of inducing proliferation and chemotaxis of primary rat lung fibroblasts (RLF).

[Antifoaming agent microembolism in patients undergoing extracorporeal circulation. Its frequency in post mortem material and its pathogenic potential in vitro].

Antifoam microembolisms in patients that undergo open heart surgery, represent a risk for postoperative complications. We decided to study its frequency in an autopsy population of patients who died after heart surgery. Forty-five patients were selected and histological sections from the kidneys were studied under light microscopy, scanning electron microscopy and X-ray microanalysis.

Lung cell toxicity experimentally induced by a mixed dust from Mexicali, Baja California, Mexico.

Lung disease caused by nonoccupational exposures to inorganic particles from the soil has been reported in several areas of the world. We tested the toxic potential of dust samples from a Mexican city (Mexicali) that is frequently affected by dust storms and is geographically related to the area of San Diego, CA, where constituents of the soil have been reported to be fibrogenic. We found that samples of Mexicali dust are a mixture of approximately 75% potassium aluminum silicates (illite) and approximately 20% silica.