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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was conducted to investigate nephritogenic tubular basement membrane antigens common to human and rat kidneys. Brown Norway (BN) rats were immunized with human renal basement membrane in complete Freund's adjuvant simultaneously with Bordetella pertussis vaccine. The immunized rats developed polyuria and increased levels of serum creatinine one week after the second immunization. Renal histology at this time revealed marked, acute tubulointerstitial nephritis with linear deposition of IgG and C3 along the tubular basement membrane and Bowman's capsule, but not along the glomerular basement membrane. Rats with this tubulointerstitial nephritis rapidly developed antibodies against renal antigens from normal BN rats such as tubular basement membrane and proximal tubule brush border, however antibodies to glomerular basement membrane appeared later. Western blotting using the same rat sera detected a 145-kDa antigen from 8 M urea-solubilized human renal basement membrane and 120-kDa, 135-kDa and 145-kDa antigens from 8 M urea-solubilized BN rat renal basement membrane. This suggests that renal basement membranes of human and rat origin have common antigens involved in the pathogenesis of tubulointerstitial nephritis.
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PMID:Induction of interstitial nephritis in rats by basement membrane of human origin. 268 56

Alterations in rat renal glucose transport following in vivo use of Freund's adjuvant were examined. Lewis-Brown Norway rats were placed in four separate injection groups: tubular basement membrane plus adjuvant [complete Freund's adjuvant (CFA) plus pertussis]; adjuvant (CFA plus pertussis); CFA only; or pertussis only. Renal handling of glucose was assessed 14 days after a single injection. No in vivo changes were noted. No histologic differences among groups were noted. However, brush border membrane vesicles prepared from animals in groups 1, 2, and 3 showed a marked decrease in glucose uptake. Further, Michaelis-Menten kinetics demonstrated a decrease in apparent Km and Vmax for glucose in groups 1, 2, and 3. CFA alone can cause a change in brush border membrane vesicle uptake of glucose. The pathogenic mechanism behind CFA-induced transport changes remains unclear. However, studies employing CFA cannot dismiss Freund's adjuvant as "inert" and must take into account functional changes created by CFA alone.
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PMID:Alterations in rat renal glucose transport following in vivo use of Freund's adjuvant. 371 53

We previously identified transcripts encoding a G protein-coupled, extracellular calcium/polyvalent cation-sensing receptor, RaKCaR, in rat kidney (D. Riccardi, J. Park, W.-S. Lee, G. Gamba, E. M. Brown, and S. C. Hebert. Proc. Natl. Acad. Sci. USA 92:131-135, 1994), which was proposed to provide the mechanism for modulating a variety of renal functions in response to changes in extracellular Ca2+ (E. M. Brown. In: Handbook of Physiology. Bethesda, MD: Am. Physiol. Soc., 1992, sect. 8, vol. 2, chapt. 39, p. 1841-1916; and S. C. Hebert. Kidney Int. 50: 2129-2139, 1996). Here, we examine the cellular and regional distribution of receptor protein by immunofluorescence microscopy using a polyclonal antibody raised against a 22 amino acid region of the NH2 terminus of the receptor. The most intense fluorescence was seen at the basolateral border of cortical thick ascending limb cells. Basolateral staining for the receptor was also detected in medullary thick ascending limbs, in macula densa cells identified by costaining with antibody to brain nitric oxide synthase, NOS-B1, and in distal convoluted tubule cells distinguished by costaining for the apical thiazide-sensitive Na(+)-Cl- cotransporter. Apical anti-RaKCaR staining was detected at the base of the brush border of proximal tubules with decreasing intensity from S1 to S3 segments. In cortical collecting ducts, anti-RaKCaR staining was detected in some, but not all, type A intercalated cells identified by costaining with anti-H(+)-ATPase and anti-AE1 Cl-/HCO3- exchanger antibodies. The present study demonstrates that RaKCaR protein is expressed in many different nephron segments and that the polarity of receptor expression varies with cell type along the nephron. These results suggest potential roles for the extracellular Ca2+/ polyvalent cation-sensing receptor in responding to both circulating and urinary concentrations of divalent minerals and potentially other polyvalent cations (e.g., aminoglycoside antibiotics) to modulate nephron function.
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PMID:Localization of the extracellular Ca2+/polyvalent cation-sensing protein in rat kidney. 953 Feb 79

Using Brown Norway (BN) rats, we isolated and characterized the tubular basement membrane (TBM) antigens that are immunologically common to humans. The renal basement membrane (RBM) of BN rat, as an antigen source, was solubilized with 8 M urea instead of collagenase followed by extraction with 0.5 M NaCl. On frozen section-immunohistochemistry, the autoantibody obtained from BN rats, which had been immunized with human RBM and showed tubulointerstitial nephritis, bound to the TBM, the basement membrane of the Bowman's capsule, and the brush border of the proximal tubules, but not to the GBM of the normal BN rat kidney. Nephritogenic antigens were isolated by immunoaffinity chromatography using Sepharose-bound purified autoantibody. By Western blot analysis of the eluate, bands with molecular weight of 200 kDa and 180 kDa were positively reacted to anti-FX1A (brush border antigen) antibody and were apparently different from the major bands with molecular weight of 145 kDa and 130 kDa. The bands with molecular weight of 145 and 130 kDa showed major cross reactivity with antibodies to fibronectin and laminin. In contrast with these high molecular weight (HMW) bands, the major 60 kDa band with three minor bands showed no reactivity with any type of antibody tested. These results indicated that the non-enzymatic solubilization of RBM is one of the possible procedures for isolating the HMW form of antigens. These antigens may be epitopically modified pre-existing constitutions of the basement membrane and may play a role in the induction of tubulointerstitial nephritis.
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PMID:Isolation and characterization of tubular basement membrane antigen common to humans and rats. 985 23

Food restriction (FR) exerts a variety of beneficial effects and may prolong life in both humans and animals. However, studies of its effects on the cortical brush border membrane (BBM) and basolateral membrane (BLM) lipid concentration, which may be pertinent to renal function, have not been reported in detail. We hypothesized that FR would decrease renal work and lower renal membrane lipid concentration. The changes in lipid concentration would be most dramatic in BBM because this membrane is the entry site for the recovery of filtered ions and nutrients. Young male Fischer 344 x Brown-Norway F1 rats consumed food ad libitum (AL) or were food-restricted (FR, 60% of AL consumption) for 6 wk. AL rats had higher fractional excretions of Na(+), K(+), and Cl(-) than did the FR group (P < 0.001). Renal Na,K-ATPase activity in AL rats was 100% higher than in FR rats (P < 0.001), reflecting greater renal work. The work required for renal proton secretion was lower in FR than in the AL rats. In FR rats, all BBM phospholipid concentrations (phosphatidylserine, phosphatidylcholine, phosphatidylethanolamine, and sphingomyelin) were approximately 50% lower than in the AL rats (P < 0.001). In the BLM, food restriction resulted only in lower phosphatidylcholine concentration, while the other phospholipids were unaffected. Plasma and renal membrane (BBM and BLM) cholesterol concentrations were significantly lower in FR than in AL rats. These results show that a nutritionally complete, but energy restricted, diet improves renal function. It also prevents renal membrane lipid deposition and decreases plasma cholesterol. Prolonged food restriction might attenuate the renal injury that occurs in obese humans as a consequence of insulin resistance and atherosclerosis.
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PMID:Food restriction beneficially affects renal transport and cortical membrane lipid content in rats. 1046 Feb 4

In order to test the hypothesis (Munn, Zhou, Attwood, Bondarev, Conway, Marshall, Brown, Mellor, Science 281 (1998) 1191-1193) that localized placental tryptophan catabolism prevents immune rejection of the mammalian fetus, the cellular localization and characteristics of human placental indoleamine 2,3-dioxygenase (EC 1.13.11.42) were studied. The localization of indoleamine 2, 3-dioxygenase activity was determined quantitatively using cell fractionation by differential and discontinuous sucrose gradient centrifugation. Enzyme activity was looked for in isolated brush border microvillous plasma membranes of placental syncytiotrophoblast. We found that this membrane preparation (which showed a 32.4-fold purification from the starting homogenate with reference to the activity of a membrane marker enzyme, alkaline phosphatase (EC 3.1.3.1)) was strongly negatively enriched with indoleamine 2,3-dioxygenase (which showed a one twenty-fifth decrease in its specific activity). Placental indoleamine 2, 3-dioxygenase is thus not expressed in the maternal facing brush border membrane of syncytiotrophoblast. 1-Methyl-DL-tryptophan which was used by Munn et al. as a key experimental tool for inhibiting indoleamine 2,3-dioxygenase in the murine model showed a competitive inhibition of human placental indoleamine 2,3-dioxygenase with L-tryptophan. The hypothesis, based on experiments performed in mouse, may therefore be applicable to avoidance of immune rejection of the fetus in human pregnancy.
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PMID:Human placental indoleamine 2,3-dioxygenase: cellular localization and characterization of an enzyme preventing fetal rejection. 1056 24