This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Pawelczyk, T. Articles by Szutowicz, A. Search for Related Content PubMed PubMed Citation Articles by Pawelczyk, T. Articles by Szutowicz, A.

(American Journal of Pathology. 2005;167:315-325.)
© 2005 American Society for Investigative Pathology

Region-Specific Alterations of Adenosine Receptors Expression Level in Kidney of Diabetic Rat

Tadeusz Pawelczyk^*, Marzena Grden^*, Robert Rzepko, Monika Sakowicz^* and Andrzej Szutowicz

From the Departments of Molecular Medicine,^* Pathomorphology, and Laboratory Medicine, Medical University of Gdansk, Gdansk, Poland

Pathological alterations of renal function in insulin-dependent diabetes have been attributed to numerous factors, including adenosine. This study examined the expression levels of adenosine receptors (ARs) in the kidney of the streptozotocin-induced diabetic rat. In the diabetic kidney A1-AR mRNA levels increased 1.7- and 2.8-fold in cortex and medulla, respectively. This was accompanied by increased A1-AR protein levels in membranes of kidney cortex (1.5-fold) and medulla (threefold). A1-AR immunoreactivity increased strongly along medullar tubules especially in the collecting duct. The levels of A2a-AR mRNA increased twofold in diabetic kidney cortex but remained unchanged in medulla; however, A2a-AR protein levels increased more than threefold in cortex. Immunohistochemistry showed increased A2a-AR immunoreactivity in luminal membranes of cortical collecting ducts and in epithelial cells of preglomerular vessels. There were no significant changes in A2b-AR expression in diabetic kidney except in medullar membranes, where the receptor protein content decreased by 60%. A3-AR mRNA levels in diabetic kidney remained unchanged, but membrane-associated A3-AR protein levels increased by 70% in diabetic kidney cortex and decreased by 80% in medulla. These changes in ARs genes expression, receptor protein content, and cellular and tissue distribution, correspond to abnormalities characteristic of the diabetic kidney, suggesting involvement in pathogenesis of diabetic nephropathy.

This article has been cited by other articles:

				S. B. Bender, J. D. Tune, L. Borbouse, X. Long, M. Sturek, and M. H. Laughlin Altered Mechanism of Adenosine-Induced Coronary Arteriolar Dilation in Early-Stage Metabolic Syndrome Exp Biol Med, June 1, 2009; 234(6): 683 - 692. [Abstract] [Full Text] [PDF]

				T. Rieg and V. Vallon ATP and adenosine in the local regulation of water transport and homeostasis by the kidney Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2009; 296(2): R419 - R427. [Abstract] [Full Text] [PDF]

				R. Faulhaber-Walter, L. Chen, M. Oppermann, S. M. Kim, Y. Huang, N. Hiramatsu, D. Mizel, H. Kajiyama, P. Zerfas, J. P. Briggs, et al. Lack of A1 Adenosine Receptors Augments Diabetic Hyperfiltration and Glomerular Injury J. Am. Soc. Nephrol., April 1, 2008; 19(4): 722 - 730. [Abstract] [Full Text] [PDF]

				Z. Guan, D. A. Osmond, and E. W. Inscho Purinoceptors in the Kidney Exp Biol Med, June 1, 2007; 232(6): 715 - 726. [Abstract] [Full Text] [PDF]

				V. Vallon, B. Muhlbauer, and H. Osswald Adenosine and kidney function. Physiol Rev, July 1, 2006; 86(3): 901 - 940. [Abstract] [Full Text] [PDF]