ORCID Profile
0000-0002-3339-2050
Current Organisation
Cardiff University
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Publisher: Springer Science and Business Media LLC
Date: 12-1987
DOI: 10.1007/BF00165755
Abstract: Endometrioid carcinoma of the ovary is one of the most types of epithelial ovarian cancer associated to endometrioisis. Endometrioid tumors as well as endometriotic implants are characterized by the presence of epithelial cells, stromal cells, or a combination of booth, that resemble the endometrial cells, suggesting a possible endometrial origin of these tumors. Pro-inflammatory cytokines, including interleukin-1 (IL-1) have been reported to be involved in both endometriosis and ovarian carcinogenesis. The major objective of this study was to determine the level expression of IL-1 ligands system (IL-1alpha, IL-1beta and IL-1RA) in the most common subtypes of ovarian cancer cells compared to endometrial cells. We used primary endometrial cells, endometrial cell line RL-952 and different subtypes of epithelial ovarian cancer cell lines including TOV-112D (endometrioid), TOV-21G (clear cell) and OV-90 (serous). Immunofluorescence and real-time PCR analysis were used respectively for detecting IL-1 ligands at the levels of cell-associated protein and mRNA. Soluble IL-1 ligands were analyzed by ELISA. We demonstrated that IL-1 ligands were expressed by all endometriosis-associated ovarian cancer subtypes and endometrial cells. In contrast to other cancer ovarian cells, endometrioid cells exhibit a specific decrease of cell-associated IL-1RA expression and its soluble secretion. Endometrioid ovarian cancer exhibits an alteration in the expression of IL-1RA, a key protector against tumorogenic effects of IL-1. This alteration evokes the same alteration observed in endometriotic cells in previous studies. This suggests a possible link between the endometrium, the tissue ectopic endometriosis and endometrioid ovarian cancer.
Publisher: Informa UK Limited
Date: 1987
DOI: 10.3109/10799898709056781
Abstract: Alpha 1- and beta-adrenoceptor responsiveness and binding have been examined in cardiac tissues removed from guinea-pigs pretreated with 6-hydroxydopamine (6-OHDA) for 3 weeks. Results were compared with control tissues from sham-injected animals. Chemical sympathectomy with 6-OHDA resulted in an increase in the sensitivity of postjunctional beta-adrenoceptor-mediated responses to isoprenaline. No such increase was observed for the alpha 1-adrenoceptor-mediated responses to methoxamine. The increase in beta-adrenergic responsiveness was accompanied by a significant (P less than 0.05) 52% increase in the number of [3H]-dihydroalprenolol binding sites with no change in binding affinity. [3H]-Prazosin binding was not affected by pretreatment with 6-OHDA. The results suggest that cardiac beta- but not alpha 1-adrenergic responsiveness is regulated by the sympathetic innervation.
Publisher: Springer Science and Business Media LLC
Date: 04-1985
DOI: 10.1007/BF00501207
Abstract: Glucocorticoids have important effects on renal function, including the modulation of renal acidification by the major proximal tubular Na(+)/H(+) exchanger, NHE3. While the chronic effect of glucocorticoids is considered to be primarily at the transcriptional level, with increases in NHE3 mRNA and protein expression driving increased transport activity, the mechanisms by which glucocorticoids activate NHE3 in an acute setting have not been investigated. Previous studies have shown that a glucocorticoid-stimulated increase in NHE3 activity can occur before any detectable change in NHE3 mRNA. The present study examines the acute effects of glucocorticoids on NHE3 using opossum kidney (OKP) cells as a cell model. In OKP cells, total NHE3 protein abundance was not changed by 3 h of treatment with dexamethasone (10(-6) M). However, the biotin-accessible fraction representing NHE3 at the apical membrane as well as Na(+)/H(+) exchange activity measured fluorimetrically using the pH-sensitive dye BCECF-AM were significantly increased. These effects were not prevented by the protein synthesis inhibitor cycloheximide. NHE3 insertion (biotinylatable NHE3 after sulfo-NHS-acetate blockade) was stimulated by dexamethasone incubation, with or without cycloheximide. The rate of NHE3 endocytic retrieval, assessed either by the avidin protection assay (early endocytosis) or by the sodium 2-mercaptoethane sulfonate (MesNa) cleavage assay (early and late endocytosis), was not affected by dexamethasone. These findings suggest that trafficking plays a key role in the acute stimulation of NHE3 by glucocorticoids, with exocytosis being the major contributor to the glucocorticoid-induced rapid increase in cell surface NHE3 protein abundance and Na(+)/H(+) exchange activity.
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Kenneth Broadley.