PubMed · 2454088
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A E Walts. 1988. Involucrin.. https://pubmed.ncbi.nlm.nih.gov/2454088/
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In ovarian cancer cells, the macrophage colony-stimulating factor-1 (CSF-1) induces the release of plasminogen activator inhibitor-2 (PAI-2), and high levels of PAI-2 as well as of CSF-1 in ovarian cancer ascites are independently correlated with poor outcome. We now study the effect of CSF-1 on PAI-2 expression in vitro and the significance of cellular PAI-2 expression in vivo. Immunohistochemical detection of PAI-2 was studied in primary and metastatic tissues from 130 epithelial ovarian cancer cases. Kaplan-Meier curves of survival were compared with the results of log-rank test. The Cox regression model was used for multivariate analysis. The effect of CSF-1 on PAI-2 expression in ovarian cancer cells was also examined in vitro. Fifty-eight percent of the primary tumors and 68% of the metastases expressed PAI-2. PAI-2 expression in the metastases of invasive stages III and IV cases was strongly predictive of a prolonged disease-free and overall survival. This finding was associated with low residual disease and was also an independent factor for disease-free survival. In vitro, CSF-1 treatment of ovarian cancer cells resulted in a decrease in cellular staining for PAI-2 while increasing the release of PAI-2 into the conditioned medium. In vivo, we also found an inverse correlation between expression of CSF-1 and that of PAI-2 in the primary tumors. We thus describe the favorable independent prognosis of cellular PAI-2 expression in the metastases of ovarian cancer. Moreover, an inverse correlation was observed between CSF-1 and PAI-2 expression in vivo. This lends support for a primary role of cell-surface (vs. secreted)-mediated events of plasminogen activation in the development of invasive, poor prognostic phenotypes.
The flux of fluid, ions, macromolecules, and inflammatory cells across airway epithelium depends in part upon the integrity of its apico-lateral tight junctions. Without the correct balance of fluid and ions, the normal functioning of mucociliary clearance and the neural responsiveness of the airways cannot take place. Freeze-fracture electron microscopy has been used to investigate the structure of human airway tight junctions and their morphology comprehensively characterised at two airway levels (main and lobar bronchi). Further data is needed to establish if the fall in transepithelial electrical resistance found across progressively proximal disparate airway generations is correlated with an alteration in tight junction morphology. Altered epithelial permeability is associated with the development of the airway conditions: asthma, chronic bronchitis, and cystic fibrosis. However, few data have been published on the structure of tight junctions in asthma and chronic bronchitis. In patients with cystic fibrosis, airways obtained at transplantation and postmortem show a basal extension of the apico lateral tight junctional belt. This change is not unique to cystic fibrosis airways as it also occurs in non-respiratory systems postmortem. However the functional relevance of these changes remains uninvestigated and recently developed in vitro models may help answer this question. The data demonstrate that tight junctions are highly dynamic structures capable of rapid alterations in disease and in response to functional stress.
Neurofilaments are the characteristic intermediate filaments of mature neurons; during development and in some neuronal cell lines and neuroendocrine tumors, neurofilament proteins are expressed together with vimentin or cytokeratins. In some cell types, the filamentous arrays formed by neurofilaments and vimentin or cytokeratins do not coincide. However, individual neurofilament proteins co-assemble with vimentin in transfected non-neuronal cells. In order to determine whether individual neurofilament proteins could also co-assemble with cytokeratins in a cellular environment, the light chain of neurofilaments, NF-L, was transfected into MCF-7 cells, in which the only cytoplasmic intermediate filament proteins expressed are cytokeratins. In transfected MCF-7 cells, human NF-L was localized to a prominent filamentous network. This pattern most probably reflected the incorporation of NF-L into the endogenous keratin cytoskeleton as it is unlikely to be due to human NF-L self-assembly since, like its rodent counterpart, human NF-L accumulated into punctate aggregates when transiently transfected in intermediate filament-deficient SW13 vim- cells. These results suggest the existence of a specific mechanism of segregation of neurofilaments and keratin filaments in some cell types.