platelet endothelial cell adhesion moleculeĮndogenous glucocorticoids modulate several physiological responses, such as glucose metabolism, cardiovascular activity and immune reactions ( Wilckens and De Rijk, 1997 Marik and Zaloga, 2002).The molecular mechanism induced by activated GR is different in each cell, as NF-κB translocation was only altered in endothelial cells.īritish Journal of Pharmacology (2007) 152, 1291–1300 doi: 10.1038/sj.bjp.0707512 published online 5 November 2007 Conclusions and implications:Įndogenous glucocorticoids, through activation of GR on neutrophils, physiologically control the rolling behaviour of these cells and, by modulating endothelial functions, affect their adhesiveness.
Membrane expressions, mRNA levels of ICAM-1, VCAM-1 and PECAM-1 and NF-κB translocation into the nucleus were higher in the endothelium of adrenalectomized and RU 38486 treated rats. P-selectin and E-selectin expression in endothelial cells was unchanged by adrenalectomy or RU 38486 treatment. RU 38486 treatment altered the maturation phases of neutrophilic lineage and reduced expression of L-selectin in mature neutrophils from bone marrow increased the number of neutrophils in the circulation and elevated the expression of L-selectin in these cells. NF-κB activity in neutrophils and endothelium was quantified by EMSA. Expressions of P-selectin, E-selectin, PECAM-1, VCAM-1 and ICAM-1 were measured by immunohistochemistry on vessels of cremaster muscle and their mRNA levels quantified in primary cultured endothelial cells. Cell numbers in bone marrow and circulation were morphologically quantified and expressions of L-selectin determined by flow cytometry. Male Wistar rats were treated with RU 38486 or adrenalectomized.
In this study the role of the glucocorticoid receptor (GR) in the physiological control of neutrophil mobilization was investigated, focusing on the specific mechanisms for mature neutrophils in bone marrow, circulating neutrophils and endothelial cells. We have shown that endogenous glucocorticoids control neutrophil mobilization in the absence of inflammation.
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