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1 Core Proteomics Laboratory, Kidney Disease Program, Department of Medicine, University of Louisville, Louisville, KY, USA
2 Core Proteomics Laboratory, Kidney Disease Program, Department of Medicine, University of Louisville, Louisville, KY, USA; Department of Biochemistry and Molecular Biology, University of Louisville, Louisville, KY, USA; Department of Medicine, Veterans Affairs Medical Center, Louisville, KY, USA
3 Department of Pharmacology and Toxicology, University of Louisville, Louisville, KY, USA
4 Department of Pathology, Jewish Hospital, Louisville, KY, USA
5 Department of Medicine, Medical University of South Carolina, Charleston, SC, USA; Department of Medicine, Ralph H. Johnson VA Medical Center, Charleston, SC, USA
* To whom correspondence should be addressed. E-mail: visith.thongboonkerd{at}louisville.edu.
Plasma sodium concentration is maintained even when sodium intake is altered. Sodium homeostasis may involve changes in renal tubular protein expression that are reflected in the urine. We used proteomic analysis to investigate changes in urinary protein excretion in response to acute sodium loading. Rats were given deionized water followed by hypertonic (2.7%) saline for 28 hours each. Urinary protein expression was determined during the final 4 hours of each treatment. Acute sodium loading increased urinary sodium excretion (4.53 ± 1.74 vs. 1.70 ± 0.27 mmol/day, p = 0.029). Urinary proteins were separated by 2-DE and visualized by SYPRO ruby staining. Differentially expressed proteins were identified by MALDI-TOF MS followed by peptide mass fingerprinting. A total of 45 protein components were changed in abundance after acute sodium loading. Neutral endopeptidase, solute carrier family 3, meprin 1
, diphor-1, chaperone HSP72, vacuolar H+-ATPase, ezrin, ERM-binding protein, glutamine synthetase, guanine nucleotide-binding protein, Rho GDI-1, and chloride intracellular channel protein 1 (CLIC-1) were decreased, whereas albumin and -2u globulin were increased. Some of these proteins have previously been shown to be associated with tubular transport. These data indicate that alterations in excretion of several urinary proteins occur during acute sodium loading.
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