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  • Title: Angiotensin II down-regulates the SR-BI HDL receptor in proximal tubular cells.
    Author: Wolf G, Wenzel U, Jablonski K, Brundert M, Rinninger F.
    Journal: Nephrol Dial Transplant; 2005 Jun; 20(6):1222-7. PubMed ID: 15894808.
    Abstract:
    BACKGROUND: The kidney plays an important role in the metabolism of lipoproteins, but renal cells are also a target of lipids under pathophysiological conditions contributing to organ damage and progression of disease. The majority of studies has focused on the interaction of renal cells with low-density lipoproteins. Relatively little is known of potential metabolism of high-density lipoproteins (HDL) on renal cells However, diverse pathophysiological situations, such as the nephrotic syndrome and acute renal injury, may be associated with an activated renin-angiotensin system as well as altered renal handling of HDL. Therefore, the present study sought to gain insight into the expression of the HDL receptor scavenger receptor class B type I (SR-BI) in cultured renal cells and a potential regulation by angiotensin II (ANG II). METHODS: Different renal cells lines and primary cultures (proximal tubular and mesangial cells) were screened by western blot for the expression of SR-BI. MCT cells, a mouse proximal tubular cell line, were selected for further studies. SR-BI protein and mRNA expression were determined after treatment with various doses of ANG II in the presence or absence of AT(1)- or AT(2)-receptor blocker. Uptake of HDL-associated cholesteryl ester into MCT cells was determined. Finally, rats were infused intraperitoneally with ANG II for 3-7 days, proximal tubules were isolated by differential centrifugation and SR-BI protein expression was assessed. Results. SR-BI protein was expressed in various primary cultures and permanent renal cell lines. ANG II (10(-10)-10(-6) M) treatment for 24 h induced a significant down-regulation of SR-BI protein and mRNA expression in MCT cells. This suppression was attenuated by an AT(1)-receptor antagonist whereas an AT(2)-blocker was without effect. MCT cells revealed a high selective uptake of HDL cholesteryl ester that was significantly higher than that in syngeneic mesangial cells. ANG II for 24 h significantly reduced this selective HDL cholesteryl ester uptake into MCT, but not mesangial cells. Finally, ANG II- infusion into rats for 3 and 7 days induced a significant decrease of SR-BI protein expression in isolated tubules. CONCLUSIONS: Our data show that ANG II mediates down-regulation of SR-BI expression on proximal tubular cells in vivo and in vitro. However, the effects were small and additional experiments are necessary to confirm these first observations. The attenuated SR-BI expression is functionally relevant and associated with a decrease in cholesteryl ester uptake. ANG II-mediated suppression may contribute to various pathophysiological situations, such as acute tubular injury, the nephrotic syndrome and atherosclerosis.
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