Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dipeptidyl peptidase IV (EC 3.4.14.5) and angiotensinase A (EC 4.4.11.7) were purified to homogeneity from pooled urine concentrate of patients with renal damage, using ultrafiltration, ammonium sulphate precipitation, lectin affinity chromatography, FPLC-ion-exchange(Mono-Q-)chromatography, and FPLC-gel filtration (Superdex). Based on the specific enzyme activity of the starting material, dipeptidyl peptidase IV was enriched 1629 fold, angiotensinase A 1183 fold. The relative molecular masses, Michaelis constants and isoelectric points were determined. Negative staining of the purified enzymes revealed globular proteins (5-7 nm). Antisera raised against dipeptidyl peptidase IV and angiotensinase A reacted specifically with tubular and, in the case of anti-angiotensinase A sera, with tubular and glomerular structures. In addition, urinary membrane vesicles of proximal tubule origin were eluted with the void volume (Superdex-gel filtration), indicating heavy epithelial cell disintegration. Both soluble tissue enzymes (dipeptidyl peptidase IV, angiotensinase A) and vacuolar blebs shed from epithelia contribute to proteinuria, as was shown in patients with glomerulonephritis, interstitial nephritis, diabetic nephropathy and, for angiotensinase A, in patients with essential arterial hypertension.
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PMID:Biochemical and immunological properties of urinary angiotensinase A and dipeptidylaminopeptidase IV. Their use as markers in patients with renal cell injury. 136 94

The aim of the present study was to investigate and quantitate the structural renal changes developing after stenosis of the renal artery. Twelve kidneys removed at operation from patients with elevated blood pressure due to stenosis of the renal artery were investigated together with three kidneys with renal artery stenosis but no clinical evidence of renovascular hypertension. Eight age-matched autopsy kidneys served as controls. Stereologic methods were used to estimate the volume fractions of different structural parameters, the volume of individual glomeruli, and the structural integrity between the glomerulus and the proximal tubule. In six of the kidneys with renal artery stenosis and in the controls, the total number of nonoccluded glomeruli was estimated. Immunohistochemical staining for epithelial membrane antigen, Tamm-Horsfall protein and lectin Arachis hypogaea was performed in order to determine whether the atrophic tubules in renal artery stenosis were of proximal or distal origin. The results showed that the volume fractions of both proximal and distal tubules had decreased in renal artery stenosis, whereas the volume fractions of the glomerular tufts and interstitium increased. Immunohistochemical staining indicated, however, that more distal than proximal tubules were preserved, although atrophic. In the kidneys with artery stenosis, very few glomeruli were seen connected to a normal proximal tubule; in 52% of the glomeruli Bowman's capsule did not open toward a tubule and 40% were connected to an atrophic tubule. The mean glomerular volume (uncorrected for shrinkage) of 1.5.10(6) microns3 in the kidneys with artery stenosis was significantly decreased compared with the 2.9.10(6) microns3 in the controls. The mean glomerular number was normal in the kidneys with artery stenosis. The study shows that despite the absence or severe atrophy of the tubules, the glomeruli are not destroyed but only smaller. More proximal than distal tubules are destroyed by the ischemic process.
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PMID:Atubular glomeruli in renal artery stenosis. 175 5

Commonly used methods for assessing reductions in microvascular density (rarefaction) in hypertension detect only perfused microvessels. In the present study, samples of cremaster and spinotrapezius muscles were taken from rats with chronic (4-week) reduced renal mass hypertension and normotensive sham-operated control rats, as well as from 12-week-old spontaneously hypertensive rats and their normotensive Wistar-Kyoto control strain. Mean arterial pressure was 149 +/- 8 mm Hg in the rats with reduced renal mass hypertension, 114 +/- 7 mm Hg in sham-operated rats, 177 +/- 9 mm Hg in spontaneously hypertensive rats, and 95 +/- 4 mm Hg in Wistar-Kyoto rats. Muscle samples were incubated with rhodamine-labeled Griffonia simplicifolia I lectin, which identifies both perfused and nonperfused microvessels. Microvascular density was assessed by counting intersections with a 20-microns grid. Microvessel density was significantly reduced in cremaster muscles of both spontaneously hypertensive and reduced renal mass hypertensive rats, and in the spinotrapezius muscle of spontaneously hypertensive rats, compared with their respective normotensive controls. Further studies in the reduced renal mass rats on low salt diets indicated that lectin binding was also decreased as salt intake was increased, independent of blood pressure. This change was not due to an alteration in lectin-binding affinity. These studies indicate that lectin binding can be a useful tool for assessing microvessel density that does not depend on the perfusion state of the vessels and that rarefaction due to hypertension is not evenly distributed in all vascular beds. These results also provide evidence that dietary salt intake alone can influence microvessel density, as measured by the lectin technique.
Hypertension 1990 Jun
PMID:Microvessel changes in hypertension measured by Griffonia simplicifolia I lectin. 235 31

Clinical histories and renal biopsies were reviewed in 12 children with acute tubulointerstitial nephritis, which was drug related in eight, idiopathic in one, and multifactorial in three. Presentation with rashes and hypertension was most common in patients with drug-associated nephritis. Eosinophils, which were present in the majority of the renal biopsies, did not distinguish between drug-related and non-drug-related disease. The majority of the children had a good outcome irrespective of the insulting agent. Frequent tubular basement membrane breaks were identified in seven of the biopsies but were not associated with a poor outcome. Proximal tubule brush border thinning, demonstrated by periodic acid-Schiff and Tetragonolobus lotus staining, paralleled the severity of acute renal failure. Lectin and immunohistochemical techniques to identify proximal tubules (Tetragonolobus lotus), thick ascending limb of Henle (anti-Tamm-Horsfall protein antibodies), and collecting ducts (Arachis hypogaea) allowed better delineation of sites of inflammation and injury, showed collecting tubules to be involved in all cases, and demonstrated that small atrophic tubules were able to maintain the ability to stain with the appropriate lectin/antibody. It is proposed that studies using these techniques may better identify the nephron sites involved in a variety of renal diseases involving tubular segments.
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PMID:Acute tubulointerstitial nephritis in children: clinical, morphologic, and lectin studies. A report of the Southwest Pediatric Nephrology Study Group. 268 4

A galactose-specific lectin, recently described by our laboratory, is immunologically demonstrable on the surface of neoplastic cells derived from patients with Hodgkin's disease. This Hodgkin's lectin is shown to be functionally and antigenically related to the galactose-N-acetylgalactosamine-specific lectin of the hepatocyte (HBP). Poly- and monoclonal antibodies against either the cytoplasmic tail or the cell-surface binding site of HBP recognize the Hodgkin's lectin as a 55 Kd protein. Expression of the 55 Kd antigen appears to be restricted to Hodgkin's disease involved tissues and cells of the monocyte/macrophage lineage. The putative identification of the Hodgkin's lectin as an ectosialyltransferase unique to Hodgkin's cells is supported by inhibition of enzymatic activity by anti-HBP antibodies. Cultured Hodgkin's cells, in analogy to purified HBP, agglutinate T-lymphocytes mediated by the Hodgkin's lectin. This cell-to-cell interaction results in the incorporation of sialic acid into lymphocyte surface asialoglycans as well as in the stimulation of lymphocyte proliferation. The function of the Hodgkin's lectin as lymphocyte agglutinant in vitro suggests its role as an immunomodulator contributing to the immunodeficiencies associated with Hodgkin's disease.
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PMID:A marker and putative pathoantigen of Hodgkin's cells. 269 Feb 34

The galactophilic lectin expressed on the surface of cultured Hodgkin's cells, recently described by this laboratory, has binding characteristics similar to those of the hepatic asialoglycoprotein receptor (HBP), and has been recognized as a Mr 55,000 (p55) membrane glycoprotein by a polyclonal antiserum to rat HBP. This study confirms the close structural relationship between the two lectins showing immunological cross-reactivity of monoclonal and polyclonal antibodies recognizing distinct epitopes on rat or human HBP. In support of the suggested dual nature of p55 as lectin and ectosialyltransferase, enzyme activity is inhibited by the monoclonal anti-HBP antibody, anti-HA 116. Cultured Hodgkin's cells, as purified HBP, agglutinate T-lymphocytes expressing hyposialylated membrane glycosyl determinants. This cell-cell interaction mediated by p55 results in the incorporation of sialic acid into lymphocyte surface asialo-glycans. The function of the Hodgkin's lectin as lymphocyte agglutinant in vitro suggests its role as an immunomodulator contributing to the immunodeficiencies associated with Hodgkin's disease.
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PMID:Hodgkin's cell lectin: an ectosialyltransferase and lymphocyte agglutinant related to the hepatic asialoglycoprotein receptor. 356 32

This study was undertaken to localize oligosaccharide residues on the endothelial luminal plasma membrane of cerebral vessels of normotensive animals and vessels permeable to horseradish peroxidase (HRP) in angiotensin-induced acute hypertension. Wistar-Furth rats were injected with HRP intravenously and hypertension was induced by an intravenous infusion of angiotensin amide. Animals were fixed 2.5, 10 and 15 min later and the HRP reaction product was demonstrated in brain slices, followed by lectin localization using the avidin-biotin-peroxidase method. Oligosaccharide residues demonstrable on the luminal plasma membrane of cerebral endothelium of normotensive controls and both permeable and nonpermeable vessels of hypertensive animals were: alpha-D-mannosyl, alpha-D-glucosyl, beta-N-acetylglucosaminyl, sialyl, beta-D-galactosyl, alpha-L-fucosyl and alpha-N-acetyl-D-galactosaminyl groups. Peanut agglutinin did not bind to the endothelium of normotensive controls or of nonpermeable vessels in hypertensive animals, but did bind to endothelium of vessels permeable to HRP 2.5 min after the onset of hypertension. At 10 min, the luminal plasma membrane of vessels regained their normal characteristics and peanut agglutinin binding was no longer demonstrable. Our studies suggest that increased cerebrovascular permeability to protein in acute hypertension is associated with loss of the terminal sialic acid groups on the luminal plasma membrane of permeable vessels. This results in the observed reduction of charge on the endothelium and an exposure of beta-D-gal-(1-3)-D-gal N-acetyl groups leads to binding of peanut agglutinin. Both alterations are rapidly reversible and no longer demonstrable 10 min after the onset of hypertension, when blood pressures reach resting levels and the blood-brain barrier is restored.
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PMID:Cerebral endothelial plasma membrane alterations in acute hypertension. 372 33

Hodgkin's disease-derived giant cell lines (HD-cells) express high levels of ectosialyltransferase activity presumed to be a galactose-specific lectin recognizing the desialylated 3-fucosyl-N-acetyllactosamine structure (X-hapten). Both the anti-X-hapten monoclonal antibody VIM-D5 and a polyclonal antiserum to another galactose-lectin, the hepatic asialoglycoprotein receptor (HBP), recognize a 55,000-mol wt HD-cell protein (Paietta, E., R. J. Stockert, A. G. Morell, V. Diehl, and P. H. Weirnik. 1986. Proc. Natl. Acad. Sci. USA. 83:3451-3455.) That the expression of the 55,000-mol wt protein is restricted to HD-cells among X-hapten positive cells lines is confirmed in this study. The 55,000-mol wt protein is shown to be present on the cell surface and intracellularly, where an additional immunocrossreactive 150,000-mol wt protein is recognized. Extraction of the 55,000 mol wt protein from HD-cell lysates by affinity chromatography results in the loss of sialyltransferase activity. While evidence for a single protein possessing both the antigenic and the enzymatic activity is not direct, these results suggest that the ectosialyltransferase unique to HD-cells is a 55,000-mol wt membrane glycoprotein possessing the X-hapten oligosaccharide.
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PMID:Unique antigen of cultured Hodgkin's cells. A putative sialyltransferase. 373 96

A mitogenic heparin-binding (reactive) lectin-like protein (HBP) was purified from the extract of a cloned rat thymic myoid cell R615B2 by a one-step procedure of affinity chromatography on a heparin--Sepharose CL-6B column. Four distinct peptide bands with molecular weights of 10,000, 13,000, 13,700, and 14,600 were detected on SDS-polyacrylamide gel electrophoresis. This protein is mitogenic at concentrations of as low as 1.1-70.0 ng/ml for peanut lectin-nonagglutinated thymocytes and splenocytes from euthymic mice and rats but not for splenocytes from nude mice. These results indicate that thymic myoid cell-derived HBP is an important signal for one particular step in T-cell differentiation.
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PMID:Mitogenic heparin-binding lectin-like protein from cloned thymic myoid cells. 380 7

We report a case of bilaterally multifocal renal oncocytomas in a patient with chronic renal disease and a long history of hypertension. Histologic study of the multiple oncocytic neoplasms with hematoxylin-eosin, periodic acid-Schiff, trichrome, and colloidal iron stains revealed novel, intracytoplasmic lumina, which were accentuated by immunoperoxidase staining with high-molecular-weight cytokeratin, epithelial membrane antigen, and Arachis hypogaea lectin. Ultrastructural studies demonstrated multiple microvilli lining the intracytoplasmic lumina. We also review the literature on bilaterally multifocal oncocytomas.
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PMID:Intracytoplasmic lumina in a case of bilaterally multifocal renal oncocytomas. 813 31


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