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1Department of Medicine, University of Sydney, Renal Research Group, Kolling Institute of Medical Research, Royal North Shore Hospital, St. Leonards, New South Wales 2065; 4School of Biomedical Sciences, University of Queensland, St. Lucia, Queensland 4072; 3Department of Anatomy and Histology, University of Sydney, New South Wales 2006, Australia; and 2Physiologisches Institut, University of Würzburg, 97070 Würzburg, Germany
Submitted 30 December 2002 ; accepted in final form 2 June 2003
The progression of renal disease correlates strongly with hypertension and the degree of proteinuria, suggesting a link between excessive Na+ reabsorption and exposure of the proximal tubule to protein. The present study investigated the effects of albumin on cell growth and Na+ uptake in primary cultures of human proximal tubule cells (PTC). Albumin (1.0 mg/ml) increased cell proliferation to 134.1 ± 11.8% (P < 0.001) of control levels with no change in levels of apoptosis. Exposure to 0.1 and 1.0 mg/ml albumin increased total 22Na+ uptake to 119.1 ± 6.3% (P = 0.005) and 115.6 ± 5.3% (P < 0.006) of control levels, respectively, because of an increase in Na+/H+ exchanger isoform 3 (NHE3) activity. This was associated with an increase in NHE3 mRNA to 161.1 ± 15.1% (P < 0.005) of control levels in response to 0.1 mg/ml albumin. Using confocal microscopy with a novel antibody raised against the predicted extracellular NH2 terminus of human NHE3, we observed in nonpermeabilized cells that exposure of PTC to albumin (0.1 and 1.0 mg/ml) increased NHE3 at the cell surface to 115.4 ± 2.7% (P < 0.0005) and 122.4 ± 3.7% (P < 0.0001) of control levels, respectively. This effect was paralleled by significant increases in NHE3 in the subplasmalemmal region as measured in permeabilized cells. These albumin-induced increases in expression and activity of NHE3 in PTC suggest a possible mechanism for Na+ retention in response to proteinuria.
proteinuria; sodium-hydrogen exchange; sodium retention
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