PubMed · 8318317
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
R S Vaughan. 1993. Double-lumen tubes.. https://doi.org/10.1093/bja%2F70.5.497
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Platelet-activating factor (PAF) plays an important role in the pathogenesis of bronchial asthma. To investigate the role of PAF in the maintenance and remodeling of the extracellular matrix, we evaluated the expression of matrix metalloproteinase-2 and matrix metalloproteinase-9 from human bronchial epithelial cells after PAF treatment. Gelatin zymography of human bronchial epithelial cell-conditioned media showed major pro-matrix metalloproteinase-9 and minor pro-matrix metalloproteinase-2 expression and these expressions were totally inhibited by the metalloproteinase inhibitor EDTA. The identification of matrix metalloproteinase-9 was confirmed by Western blot analysis. Northern blotting and zymography demonstrated that PAF induced the mRNA of matrix metalloproteinase-9 from human bronchial epithelial cells and an increase in the gelatinolytic activity of pro-matrix metalloproteinase-9 but not in that of pro-matrix metalloproteinase-2. Lyso-PAF did not induce matrix metalloproteinase-9 mRNA or the gelatinolytic activity of pro-matrix metalloproteinase-9. CV6209, an receptor antagonist of PAF, reduced the increases of pro-matrix metalloproteinase-9 mRNA and gelatinolytic activity induced by PAF. Another receptor antagonist of PAF, hexanolamine PAF, did not inhibit the increases in the synthesis or release of pro-matrix metalloproteinase induced by PAF. Based on these results, we propose that matrix metalloproteinase-9 may be actively involved in the PAF-induced physiopathological remodeling in human bronchial epithelial cells.
Analysis of the host response to viral infection generally has focused on the capacity of viruses to activate or repress transcription of cellular genes, and this approach is also characteristic of work on RNA viruses such as respiratory syncytial virus (RSV). In the present study, it appeared initially that RSV-driven expression of a critical immune regulator, the beta-chemokine RANTES (regulated upon activation, normal T cell expressed and secreted), in primary-culture airway epithelial cells also depended on inducible gene transcription because expression was accompanied by coordinate increases in transcriptional initiation rate and gene promoter activity. However, RSV-driven increases in RANTES gene transcription and promoter activity were small and transient relative to RANTES expression, and they were no different in size and duration than for inactivated RSV that was incapable of fully inducing RANTES expression. These findings suggested that the increase in RANTES gene transcription was not sufficient for inducible expression and that critical regulatory effects occurred at a posttranscriptional level. This type of mechanism for virus-inducible expression of RANTES was established when we found that replicating (but not inactivated) RSV markedly increased RANTES mRNA half-life (from 0.8 to 6.8 h). In addition, RNase protection assays of heterologous promoter/reporter plasmids indicate that basal instability of RANTES mRNA is mediated at least in part by nucleotides 11-389 of the RANTES gene, and this region is also the target for induction by virus. The distinct pathway for production of RANTES (in combination with cytokine-dependent expression of RANTES and related immune-response genes) may more effectively coordinate immune cell interaction with epithelial barrier cells to mediate host defense.
Explore the source record for details and available documents.