Inducible isoforms of cyclooxygenase and nitric-oxide synthase in inflammation.
- J. Vane, J. Mitchell, D. Willoughby
- Biology, MedicineProceedings of the National Academy of Sciences…
- 15 March 1994
The rise in COX and NOS activities in the skin during the acute phase reinforces the proinflammatory role for prostanoids and suggests one also for nitric oxide and there may be differential regulation of these enzymes, perhaps due to the changing pattern of cytokines during the inflammatory response.
Aberrant inflammation and resistance to glucocorticoids in Annexin 1−/− Mouse
It is reported that mice lacking the Anx‐1 gene exhibit a complex phenotype that includes an altered expression of other annexins as well as of COX‐2 and cPLA2 in response to carrageenin‐ or zymosan‐induced inflammation.
Glucocorticoids act within minutes to inhibit recruitment of signalling factors to activated EGF receptors through a receptor‐dependent, transcription‐independent mechanism
The results point to an unsuspected rapid effect of glucocorticoids, mediated by occupation of GR but not by changes in gene transcription, which is brought about by competition between LC1 and Grb2 leading to a failure of recruitment off signalling factors to EGF‐R.
A novel role for phospholipase A2 isoforms in the checkpoint control of acute inflammation
- D. Gilroy, Justine Newson, P. Sawmynaden, D. Willoughby, J. Croxtall
- BiologyFASEB journal : official publication of the…
- 1 March 2004
It is shown that type VI iPLA2 drives the onset of acute pleurisy through the synthesis of PGE2, LTB4, PAF, and IL‐1β, and during resolution there is a switch to a sequential induction of first sPLA2 that mediates the release of PAF and lipoxin A4.
Lipocortin 1 mediates dexamethasone-induced growth arrest of the A549 lung adenocarcinoma cell line.
The generation of prostaglandin E2 by A549 cells seems to be an important regulator of cell proliferation in vitro and the dexamethasone-induced suppression of proliferation in this model is attributable to eicosanoid inhibition caused by lipocortin 1.
Different glucocorticoids vary in their genomic and non‐genomic mechanism of action in A549 cells
- J. Croxtall, P. V. van Hal, Q. Choudhury, D. Gilroy, R. Flower
- Biology, MedicineBritish Journal of Pharmacology
- 1 January 2002
There is clear evidence of two entirely separate mechanisms of glucocorticoid action, one of which correlates with NF‐κB mediated genomic actions whilst the other, depends upon rapid effects on a cell signalling system which does not require dissociation of GR.
Investigation into the involvement of phospholipases A2 and MAP kinases in modulation of AA release and cell growth in A549 cells
- Q. Choudhury, Diane T Mckay, R. Flower, J. Croxtall
- BiologyBritish journal of pharmacology
- 1 September 2000
The results confirm that the liberation of AA release, generation of PGE2 and cell proliferation is mediated largely through the actions of cPLA2 whereas, sPLA2 plays no significant role and propose that selective inhibitors of MEK and MAPK pathways may be useful in controlling AA release.
Vildagliptin: a review of its use in the management of type 2 diabetes mellitus.
Oral vildagliptin in combination with metformin, a sulfonylurea or a thiazolidinedione improved glycaemic control in adults with type 2 diabetes and appeared to slow the progression of beta-cell degeneration in trials of 24-52 weeks' duration.
Etravirine: a review of its use in the management of treatment-experienced patients with HIV-1 infection.
- J. Croxtall
- 16 April 2012
In highly treatment-experienced patients with HIV-1 infection and evidence of viral replication, the addition of etravirine to an optimized background therapy (OBT) regimen provides an effective and well tolerated treatment that leads to improvements in both virological and immunological outcomes.
Mobilizing lipocortin 1 in adherent human leukocytes downregulates their transmigration
- M. Perretti, J. Croxtall, S. K. Wheller, N. Goulding, R. Hannon, R. Flower
- BiologyNature Network Boston
- 1 November 1996
It is reported that LCI is mobilized and externalized following PMN adhesion to endothelial monolayers in vitro or to venular endothelium in vivo and that the end point of this process is a negative regulation of PMN transendothelial passage.