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Reduced IP receptors in STZ-induced diabetic rat kidneys and high-glucose-treated mesangial cells

Department of Cellular and Molecular Medicine and Kidney Research Centre, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada K1H 8M5

Submitted 23 January 2004 ; accepted in final form 21 May 2004

Mesangial cells (MG) are an important source of renal PGE₂ and PGI₂. The purpose of this study was to examine the effects of cicaprost (CCP; PGI₂ analog) on MG function and the expression of IP receptors in streptozotocin (STZ)-diabetic rats and glucose-treated MG cells. CCP increased cellular cAMP in immortalized rat MG cells. Both glucose and anisomycin attenuated CCP-cAMP, but not PMA, angiotensin II, or transforming growth factor-. Also, IP receptor protein was reduced in response to glucose. While CCP decreased the levels of the cell cycle inhibitor p27, it did not alter thymidine or leucine incorporation. However, CCP reduced fibronectin levels by 40% and increased matrix metalloproteinase-2 levels threefold, a key enzyme in matrix degradation. Finally, IP receptors were significantly reduced in the outer medulla of 4- and 12-wk STZ-diabetic rats and in the cortex, outer, and inner medullary regions in 6-mo uninephrectomized STZ-diabetic rats. The changes in the CCP/IP system observed in this study suggest that IP may serve as an alternate therapeutic target in diabetes.

cAMP; cicaprost/IP; immortalized mesangial cells; streptozotocin-diabetic rats

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