Physiological roles for ecto-5′-nucleotidase (CD73)

被引：420

作者：

Colgan S.P. ^{[1
]}

Eltzschig H.K. ^{[1
,2
]}

Eckle T. ^{[2
]}

Thompson L.F. ^{[3
]}

机构：

[1] Center for Experimental Therapeutics, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, Thorn Building 704

[2] Department of Anesthesiology and Intensive Care Medicine, Tübingen University Hospital, Tübingen

[3] Immunobiology and Cancer Program, Oklahoma Medical Research Foundation, Oklahoma City

来源：

Purinergic Signalling | 2006年 / 2卷 / 2期

基金：

美国国家卫生研究院;

关键词：

Endothelia; Epithelia; Hypoxia; Inflammation; Nucleotidase; Nucleotide;

D O I：

10.1007/s11302-005-5302-5

中图分类号：

学科分类号：

摘要：

Nucleotides and nucleosides influence nearly every aspect of physiology and pathophysiology. Extracellular nucleotides are metabolized through regulated phosphohydrolysis by a series of ecto-nucleotidases. The formation of extracellular adenosine from adenosine 5′-monophosphate is accomplished primarily through ecto-5′-nucleotidase (CD73), a glycosyl phosphatidylinositol-linked membrane protein found on the surface of a variety of cell types. Recent in vivo studies implicating CD73 in a number of tissue protective mechanisms have provided new insight into its regulation and function and have generated considerable interest. Here, we review contributions of CD73 to cell and tissue stress responses, with a particular emphasis on physiologic responses to regulated CD73 expression and function, as well as new findings utilizing Cd73-deficient animals. © Springer 2006.

引用

页码：351 / 360

页数：9

共 87 条

[1] Zimmerman H., 5′-nucleotidase: Molecular structure and functional aspects, Biochem J, 285, pp. 345-365, (1992)
[2] Linden J., Molecular approach to adenosine receptors: Receptor-mediated mechanisms of tissue protection, Annu Rev Pharmacol Toxicol, 41, pp. 775-787, (2001)
[3] Hunsucker S.A., Mitchell B.S., Spychala J., The 5′-nucleotidases as regulators of nucleotide and drug metabolism, Pharmacol Ther, 107, pp. 1-30, (2005)
[4] Gamba G., Molecular physiology and pathophysiology of electroneutral cation-chloride cotransporters, Physiol Rev 2005, 85, pp. 423-493
[5] Madara J.L., Patapoff T.W., Gillece-Castro B., Et al., 5′-adenosine monophosphate is the neutrophil-derived paracrine factor that elicits chloride secretion from T84 intestinal epithelial cell monolayers, J Clin Invest, 91, pp. 2320-2325, (1993)
[6] Strohmeier G.R., Lencer W.I., Patapoff T.W., Et al., Surface expression, polarization, and functional significance of CD73 in human intestinal epithelia, J Clin Invest, 99, pp. 2588-2601, (1997)
[7] Thompson L.F., Eltzschig H.K., Ibla J.C., Et al., Crucial role for ecto-5′-vascular leak during hypoxia, J Exp Med, 200, pp. 1395-1405, (2004)
[8] Dejana E., Spagnuolo R., Bazzoni G., Interendothelial junctions and their role in the control of angiogenesis, vascular permeability and leukocyte transmigration, Thromb Haemost, 86, pp. 308-315, (2001)
[9] Ley K., Plugging the leaks, Nat Med, 7, pp. 1105-1106, (2001)
[10] Lennon P.F., Taylor C.T., Stahl G.L., Colgan S.P., Neutrophil-derived 5′-adenosine monophosphate promotes endothelial barrier function via CD73-mediated conversion to adenosine and endothelial A<sub>2B</sub> receptor activation, J Exp Med, 188, pp. 1433-1443, (1998)

← 1 2 3 4 5 6 7 8 9 →