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Ascorbic acid prevents oxidant-induced increases in endothelial permeability.
May JM, Qu ZC
(2011) Biofactors 37: 46-50
MeSH Terms: Antioxidants, Ascorbic Acid, Buthionine Sulfoximine, Cell Line, Endothelial Cells, Glutamate-Cysteine Ligase, Glutathione, Humans, Hydrogen Peroxide, Inulin, Oxidants, Permeability, Vitamin K 3
Show Abstract · Added December 5, 2013
Oxidative stress acutely increases the permeability of the vascular endothelium to large molecules that would not otherwise cross the barrier. Ascorbic acid is an antioxidant that tightens the endothelial permeability barrier, so we tested whether it might also prevent the increase in endothelial permeability due to cellular oxidative stress. Treatment of EA.hy926 endothelial cells cultured on filter inserts with H(2) O(2) , menadione, and buthionine sulfoximine increased endothelial permeability to radiolabeled inulin. Short-term ascorbate loading of the cells to what are likely physiologic concentrations of the vitamin by treating them with dehydroascorbate prevented the increase in endothelial permeability due to these agents. The nonphysiologic antioxidants dithiothreitol and tempol also prevented increases in endothelial barrier permeability induced by the agents. These results suggest that oxidative stress induced directly by oxidants or indirectly by glutathione depletion impairs endothelial barrier function and that intracellular ascorbate may serve to prevent this effect.
Copyright © 2010 International Union of Biochemistry and Molecular Biology, Inc.
1 Communities
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13 MeSH Terms
Probiotics ameliorate the hydrogen peroxide-induced epithelial barrier disruption by a PKC- and MAP kinase-dependent mechanism.
Seth A, Yan F, Polk DB, Rao RK
(2008) Am J Physiol Gastrointest Liver Physiol 294: G1060-9
MeSH Terms: Bacterial Proteins, Butadienes, Caco-2 Cells, Cadherins, Dose-Response Relationship, Drug, Electric Impedance, HT29 Cells, Humans, Hydrogen Peroxide, Indoles, Intestinal Mucosa, Inulin, Lactobacillus rhamnosus, Membrane Proteins, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Mitogen-Activated Protein Kinases, Nitriles, Occludin, Permeability, Phosphoproteins, Probiotics, Protein Kinase C, Protein Kinase C beta, Protein Kinase C-epsilon, Protein Kinase Inhibitors, Protein Transport, Pyrroles, Tight Junctions, Time Factors, Zonula Occludens-1 Protein, beta Catenin
Show Abstract · Added May 19, 2014
Probiotics promote intestinal epithelial integrity and reduce infection and diarrhea. We evaluated the effect of Lactobacillus rhamnosus GG-produced soluble proteins (p40 and p75) on the hydrogen peroxide-induced disruption of tight junctions and barrier function in Caco-2 cell monolayers. Pretreatment of cell monolayers with p40 or p75 attenuated the hydrogen peroxide-induced decrease in transepithelial resistance and increase in inulin permeability in a time- and dose-dependent manner. p40 and p75 also prevented hydrogen peroxide-induced redistribution of occludin, ZO-1, E-cadherin, and beta-catenin from the intercellular junctions and their dissociation from the detergent-insoluble fractions. Both p40 and p75 induced a rapid increase in the membrane translocation of PKCbetaI and PKCepsilon. The attenuation of hydrogen peroxide-induced inulin permeability and redistribution of tight junction proteins by p40 and p75 was abrogated by Ro-32-0432, a PKC inhibitor. p40 and p75 also rapidly increased the levels of phospho-ERK1/2 in the detergent-insoluble fractions. U0126 (a MAP kinase inhibitor) attenuated the p40- and p75-mediated reduction of hydrogen peroxide-induced tight junction disruption and inulin permeability. These studies demonstrate that probiotic-secretory proteins protect the intestinal epithelial tight junctions and the barrier function from hydrogen peroxide-induced insult by a PKC- and MAP kinase-dependent mechanism.
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32 MeSH Terms
Juxtacrine activation of EGFR regulates claudin expression and increases transepithelial resistance.
Singh AB, Sugimoto K, Dhawan P, Harris RC
(2007) Am J Physiol Cell Physiol 293: C1660-8
MeSH Terms: Animals, Antibodies, Antigens, CD, Autocrine Communication, Calcium, Cell Line, Cell Membrane Permeability, Dogs, Electric Impedance, Epithelial Cells, ErbB Receptors, Heparin-binding EGF-like Growth Factor, Humans, Integrin beta1, Intercellular Signaling Peptides and Proteins, Inulin, Membrane Glycoproteins, Membrane Proteins, Phosphatidylinositol 3-Kinases, Phosphoinositide-3 Kinase Inhibitors, Phosphorylation, Protein Kinase Inhibitors, Proto-Oncogene Proteins c-akt, Rats, Sodium, Tetraspanin 29, Tight Junctions, Time Factors, Transfection, Tritium
Show Abstract · Added August 19, 2013
Heparin-binding (HB)-EGF, a ligand for EGF receptors, is synthesized as a membrane-anchored precursor that is potentially capable of juxtacrine activation of EGF receptors. However, the physiological importance of such juxtacrine signaling remains poorly described, due to frequent inability to distinguish effects mediated by membrane-anchored HB-EGF vs. mature "secreted HB-EGF." In our studies, using stable expression of a noncleavable, membrane-anchored rat HB-EGF isoform (MDCK(rat5aa) cells) in Madin-Darby canine kidney (MDCK) II cells, we observed a significant increase in transepithelial resistance (TER). Similar significant increases in TER were observed on stable expression of an analogous, noncleavable, membrane-anchored human HB-EGF construct (MDCK(human5aa) cells). The presence of noncleavable, membrane-anchored HB-EGF led to alterations in the expression of selected claudin family members, including a marked decrease in claudin-2 in MDCK(rat5aa) cells compared with the control MDCK cells. Reexpression of claudin-2 in MDCK(rat5aa) cells largely prevented the increases in TER. Ion substitution studies indicated decreased paracellular ionic permeability of Na(+) in MDCK(rat5aa) cells, further indicating that the altered claudin-2 expression mediated the increased TER seen in these cells. In a Ca(2+)-switch model, increased phosphorylation of EGF receptor and Akt was observed in MDCK(rat5aa) cells compared with the control MDCK cells, and inhibition of these pathways inhibited TER changes specifically in MDCK(rat5aa) cells. Therefore, we hypothesize that juxtacrine activation of EGFR by membrane-anchored HB-EGF may play an important role in the regulation of tight junction proteins and TER.
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30 MeSH Terms
MAPK interacts with occludin and mediates EGF-induced prevention of tight junction disruption by hydrogen peroxide.
Basuroy S, Seth A, Elias B, Naren AP, Rao R
(2006) Biochem J 393: 69-77
MeSH Terms: Caco-2 Cells, Epidermal Growth Factor, Humans, Hydrogen Peroxide, Inulin, Membrane Proteins, Mitogen-Activated Protein Kinases, Occludin, Oxidative Stress, Phosphoproteins, Protein Binding, Tight Junctions, Zonula Occludens-1 Protein
Show Abstract · Added February 25, 2014
The MAPK (mitogen-activated protein kinase) pathway is a major intracellular signalling pathway involved in EGF (epithelial growth factor) receptor-mediated cell growth and differentiation. A novel function of MAPK activity in the mechanism of EGF-mediated protection of TJs (tight junctions) from H2O2 was examined in Caco-2 cell monolayers. EGF-mediated prevention of H2O2-induced increase in paracellular permeability was associated with the prevention of H2O2-induced Tyr-phosphorylation, Thr-dephosphorylation and cellular redistribution of occludin and ZO-1 (zonula occludin-1). EGF also prevented H2O2-induced disruption of the actin cytoskeleton and the dissociation of occludin and ZO-1 from the actin-rich detergent-insoluble fractions. MEK (MAPK/ERK kinase, where ERK stands for extracellular signal related kinase) inhibitors, PD98059 and U0126, completely blocked these protective effects of EGF on TJs. EGF rapidly increased the levels of phosphorylated MEK (p-MEK) in detergent-soluble fractions and phosphorylated ERK (p-ERK) in detergent-insoluble fractions. p-ERK was colocalized and co-immunoprecipitated with occludin. GST (glutathione S-transferase) pull-down assay showed that the C-terminal tail of occludin binds to p-ERK in Caco-2 cell extracts. Pair-wise binding studies using recombinant proteins demonstrated that ERK1 directly interacts with the C-terminal tail of occludin. Therefore the present study shows that ERK interacts with the C-terminal region of occludin and mediates the prevention of H2O2-induced disruption of TJs by EGF.
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13 MeSH Terms
Serial determination of glomerular filtration rate in conscious mice using FITC-inulin clearance.
Qi Z, Whitt I, Mehta A, Jin J, Zhao M, Harris RC, Fogo AB, Breyer MD
(2004) Am J Physiol Renal Physiol 286: F590-6
MeSH Terms: Animals, Consciousness, Diabetes Mellitus, Experimental, Female, Fluorescein-5-isothiocyanate, Fluorescent Dyes, Glomerular Filtration Rate, Injections, Inulin, Kidney Function Tests, Male, Mice, Mice, Inbred C57BL, Nephrectomy
Show Abstract · Added August 19, 2013
Two nonradioactive methods for determining glomerular filtration rate (GFR) in conscious mice using FITC-labeled inulin (FITC-inulin) were evaluated. The first method measured GFR using clearance kinetics of plasma FITC-inulin after a single bolus injection. Based on a two-compartment model, estimated GFR was 236.69 +/- 16.55 and 140.20 +/- 22.27 microl/min in male and female C57BL/6J mice, respectively. Total or (5/6) nephrectomy reduced inulin clearance to 0 or 32.80 +/- 9.32 microl/min, respectively. Conversely, diabetes mellitus induced by streptozotocin was associated with increased GFR. The other approach measured urinary inulin clearance using intraperitoneal microosmotic pumps to deliver FITC-inulin and metabolic cages to collect timed urine samples. This approach yielded similar GFR values of 211.11 +/- 26.56 and 157.36 +/- 20.02 microl/min in male and female mice, respectively. These studies demonstrate the feasibility of repeated nonisotopic measurement of inulin clearance in conscious mice.
1 Communities
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14 MeSH Terms
Impaired renal mevalonate metabolism in nephrotic syndrome: a stimulus for increased hepatic cholesterogenesis independent of GFR and hypoalbuminemia.
Golper TA, Swartz SH
(1982) Metabolism 31: 471-6
MeSH Terms: Animals, Cholesterol, Glomerular Filtration Rate, Inulin, Kidney, Liver, Male, Mevalonic Acid, Nephrotic Syndrome, Puromycin Aminonucleoside, Rats, Rats, Inbred Strains, Serum Albumin, Sodium
Show Abstract · Added August 10, 2015
Increased hepatic lipogenesis in the nephrotic syndrome is not adequately explained by hypoalbuminemia. In this disorder an enhanced delivery of the cholesterol precursor mevalonic acid (MVA) to the liver may be an unidentified stimulus to cholesterogenesis. Since the kidneys are the major site of mevalonate excretion and metabolism by either the sterol or nonsterol shunt pathways, an impairment of any of these metabolic alternatives could result in redistribution of mevalonate to the liver. Male Sprague-Dawley rats rendered nephrotic by puromycin aminonucleoside had their kidneys perfused with Krebs-Henseleit-bicarbonate buffer containing albumin, glucose and 5-14C-MVA. The number five carbon label was utilized so that any 14CO2 produced would represent mevalonate shunt pathway activity. The isolated perfused kidney was used to eliminate confounding variables. In eight control kidneys perfused for 2 hr 62 +/- 2% of the MVA was removed from the perfusate compared to 50 +/- 2% in five nephrotic kidneys (p less than .006). Urinary MVA recovery was 22 +/- 2% in controls. 15 +/- 1% in nephrotics (p less than .05). The incorporation of 14C into renal tissue lipids was not different in the two groups. Recovery of 14CO2 was two times greater in controls than in nephrotics (p less than .006). Inulin clearance per gram of kidney and sodium reabsorption were similar for the two groups. Isolated perfused kidneys from nephrotic rats metabolize MVA abnormally such that less is excreted, less is oxidized, and more is available for recirculation to the liver. This occurs independently of hypoalbuminemia, a change in glomerular filtration rate, or an overt histo-pathologic lesion. These events create an environment for increased hepatic cholesterol synthesis.
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14 MeSH Terms
Adaptation of Na+-H+ exchange in renal microvillus membrane vesicles. Role of dietary protein and uninephrectomy.
Harris RC, Seifter JL, Brenner BM
(1984) J Clin Invest 74: 1979-87
MeSH Terms: Animals, Biological Transport, Active, Blood Gas Analysis, Blood Urea Nitrogen, Body Weight, Dietary Proteins, Glomerular Filtration Rate, Hydrogen, Inulin, Kidney, Kinetics, Male, Membranes, Microvilli, Nephrectomy, Organ Size, Rats, Rats, Inbred Strains, Sodium
Show Abstract · Added January 28, 2014
The ablation of renal mass and institution of a high protein diet both lead to renal cortical hypertrophy and increased glomerular filtration rate (GFR). We studied Na+ transport in rat microvillus membrane vesicles isolated from uninephrectomized or sham operated rats fed 6% (low), 24% (standard), or 40% (high) protein diets. The feeding of high protein, as compared with low protein, was associated with a 50% increase in rates of pH-stimulated 22Na+ transport in isolated vesicles from sham and uninephrectomized animals. Values for the standard protein diet were intermediate to values for high and low protein. At each level of dietary protein intake, vesicular Na+ transport was greater in the uninephrectomized than in sham rats. The high protein diet was also associated with increased vesicular 22Na+ flux inhibitable by 1 mM amiloride. Increases in total and amiloride sensitive flux were also noted in the absence of a pH gradient. Conductive Na+ and H+ transport were not altered, nor were sodium-glucose and sodium-alanine cotransport. Kinetic studies revealed evidence for an increased Vmax of Na+-H+ exchange in uninephrectomized animals fed a 40 vs. a 6% protein diet whereas Km was unchanged. Supplements of NaHCO3 in the 40% protein diet, to adjust for an increased rate of net acid excretion, did not prevent the increased rates of Na+-H+ exchange. However, treatment with actinomycin D (0.12 mg/kg) prevented the increased Na+-H+ activity as well as the increased renal mass and GFR noted 24 h after unilateral nephrectomy. Na+-H+ exchange rate was closely correlated with GFR (r = 0.961; P less than 0.005) and renal mass (r = .986; P less than 0.001). These observations provide evidence for modification of the luminal membrane Na+-H+ exchanger in response to changes in dietary protein content and nephron number.
1 Communities
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19 MeSH Terms
Metabolic and functional consequences of inhibiting adenosine deaminase during renal ischemia in rats.
Stromski ME, van Waarde A, Avison MJ, Thulin G, Gaudio KM, Kashgarian M, Shulman RG, Siegel NJ
(1988) J Clin Invest 82: 1694-9
MeSH Terms: Adenosine Deaminase Inhibitors, Adenosine Triphosphate, Animals, Coformycin, Inulin, Ischemia, Kidney, Magnetic Resonance Spectroscopy, Male, Nucleoside Deaminases, Pentostatin, Rats, Rats, Inbred Strains
Show Abstract · Added December 10, 2013
The concentrations of renal ATP have been measured by 31P-nuclear magnetic resonance (NMR) before, during, and after bilateral renal artery occlusion. Using in vivo NMR, the initial postischemic recovery of ATP increased with the magnitude of the residual nucleotide pool at the end of ischemia. ATP levels after 120 min of reflow correlated with functional recovery at 24 h. In the present study the effect of blocking the degradation of ATP during ischemia upon the postischemic restoration of ATP was investigated. Inhibition of adenosine deaminase by 80% with the tight-binding inhibitor 2'-deoxycoformycin led to a 20% increase in the residual adenine nucleotide pool. This increased the ATP initial recovery after 45 min of ischemia from 52% (in controls) to 62% (in the treated animals), as compared to the basal levels. The inhibition also caused an accelerated postischemic restoration of cellular ATP so that at 120 min it was 83% in treated rats vs. 63% in untreated animals. There was a corresponding improvement in the functional recovery from the insult (increase of 33% in inulin clearance 24 h after the injury). Inhibition of adenosine deaminase during ischemia results in a injury similar to that seen after a shorter period of insult.
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13 MeSH Terms
Backtransport of dialysate solutes during in vitro continuous arteriovenous hemodialysis.
Golper TA, Leone M
(1989) Blood Purif 7: 223-9
MeSH Terms: Dialysis Solutions, Humans, Inulin, Renal Dialysis, Ultrafiltration
Show Abstract · Added August 10, 2015
Simulated continuous arteriovenous hemodialysis (CAVHD) was performed with Renaflo anisotropic polysulfone capillary hemofilters and Biospal homogeneous PAN parallel-plate hemofilters. Inulin and glucose were present in the dialysis solution. Plasma and dialysis solution flow rates were varied as was the delivery of dialysis solution by gravity or pump. The presence of dialysis solution did not affect the components of transmembrane pressure and did not alter ultrafiltration rate. Inulin and glucose backtransported into the plasma perfusate during CAVHD with the Biospal but not with the Renaflo filters. Dialysis solution will need to be sterile and pyrogen-free even in the low-flow, low-pressure system of CAVHD.
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5 MeSH Terms
The effect of tobramycin on the renal handling of vancomycin.
Munar MY, Elzinga L, Brummett R, Golper TA, Bennett WM
(1991) J Clin Pharmacol 31: 618-23
MeSH Terms: Adult, Audiometry, Creatinine, Drug Combinations, Drug Interactions, Female, Hearing Disorders, Humans, Inulin, Kidney, Male, Metabolic Clearance Rate, Tobramycin, Vancomycin, p-Aminohippuric Acid
Show Abstract · Added August 7, 2015
Studies in experimental animals and humans have suggested that enhanced renal and auditory toxicity occur with concurrent vancomycin and aminoglycoside treatment. In volunteers, systemic vancomycin clearance at steady-state was measured simultaneously with renal clearances of vancomycin, creatinine, inulin, and para-aminohippurate. Group 1 (n = 9) received vancomycin 5 mg/kg IV for 1 hour, then 1.1 mg/kg/hr for 3 hours. Group II (n = 7) received vancomycin plus tobramycin (2 mg/kg IV over 30 min). Groups did not differ demographically. Audiograms were obtained before and after vancomycin. Plasma samples were collected serially for vancomycin and tobramycin pharmacokinetic studies. Serum concentration versus time data were fit to a two-compartment model for vancomycin and a one-compartment model for tobramycin. For all volunteers, creatinine, inulin and para-aminohippurate clearance, and audiograms were not altered from baseline and were not statistically different between groups. No significant effect of tobramycin on vancomycin pharmacokinetics was observed. conversely, vancomycin had no significant effect on tobramycin pharmacokinetics. The nephrotoxic synergism of vancomycin and tobramycin is not explained by short-term differences in renal handling.
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15 MeSH Terms