The annexin-1 knockout mouse: what it tells us about the inflammatory response

• Autorzy: Roviezzo F. , Getting S.J. , Paul-Clark M.J. , Yona S. , Gavins F.N.E. , Perretti M. , Hannon R. , Croxtall J.D. , Buckingham J.C. , Flower R.J.
• Języki publikacji: EN

Abstrakty

EN

The 37kDa protein annexin 1 (Anx-1; lipocortin 1) is a glucocorticoid-regulated protein that has been implicated in the regulation of phagocytosis, cell signalling and proliferation, and postulated to be a mediator of glucocorticoids action in inflammation and in the control of anterior pituitary hormone release. Immuno-neutralisation or antisense strategies support this hypothesis as they can reverse the effect of glucocorticoids in several systems. We recently generated a line of mice lacking the Anx-1 gene noting that some tissues taken from such animals exhibited an increased expression of several proteins including COX-2 and cPLA2. In models of experimental inflammation, Anx-1-/- mice exhibit an exaggerated response and a partial or complete resistance to the anti-inflammatory effects of glucocorticoids. Several other anomalies were noted including abnormal leukocyte adhesion molecule expression, an increased spontaneous migratory behaviour of PMN in Anx-1-/- mice and a resistance in Anx-1-/- macrophages to glucocorticoid inhibition of superoxide generation. This paper reviews these and other data in the light of the development of the ‚second messenger™ hypothesis of glucocorticoid action.

Słowa kluczowe

EN

glucocorticoid; cellular signalling; transgenic animal model; phagocytosis; mouse; proliferation; inflammatory response; mice; inflammation; annexin 1

• Wydawca: -
• Czasopismo: Journal of Physiology and Pharmacology
• Rocznik: 2002
• Tom: 53
• Numer: 4,1
• Opis fizyczny: p.541-553,fig.

Twórcy

autor

Roviezzo F.

• University of London, London, U.K.

autor

Getting S.J.

autor

Paul-Clark M.J.

autor

Yona S.

autor

Gavins F.N.E.

autor

Perretti M.

autor

Hannon R.

autor

Croxtall J.D.

autor

Buckingham J.C.

autor

Flower R.J.