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  • 1
    Electronic Resource
    Electronic Resource
    Transcytosis in cultured proximal tubular cells (1986)
    Springer
    The journal of membrane biology 93 (1986), S. 237-247 
    Details
    ISSN: 1432-1424
    Keywords: pinocytosis ; proximal tubule ; Lucifer Yellow ; quin-2 ; 1-oleoyl-2-acetyl-glycerol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Studies were designed to examine fluid-phase pinocytosis in proximal tubular cells. Canine proximal tubules were obtained from the band IV of Percoll® gradient centrifugation of the dispersed renal cortex, and were seeded on collagen-coated polycarbonate membranes. Integrity of monolayers was confirmed by electrophysiologic measurements, and by scanning electron microscopy. At confluence cell monolayers were studied in Ussing chambers. The rate of transfer of a marker of fluidphase pinocytosis, Lucifer Yellow CH, from the luminal to the basolateral bath was three times higher than that occurring in the opposite direction. Fluorescence microscopy demonstrated that Lucifer Yellow was trapped exclusively in the vesicular compartment. Electron microscopy of the monolayers incubated with cationized ferritin added to the luminal or to the basolateral bath revealed that endocytic vesicles were formed only at the luminal surface. Luminal-to-basolateral transfer of Lucifer Yellow was almost completely blocked at 0°C, and was significantly diminished by K+ depletion. Transcytosis of Lucifer Yellow was stimulated twofold by 1-oleoyl-2-acetyl-glycerol. Transfer of quin-2 acetoxymethylester across the monolayer was used as a marker of the paracellular pathway, demonstrating the lack of directional selectivity of this transport route. In summary, vectorial fluid-phase pinocytosis in proximal tubular cells represents an additional mechanism contributing to fluid transport in this segment of the nephron.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01871178
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  • 2
    Electronic Resource
    Electronic Resource
    Parathyroid hormone-induced changes of the brush border topography and cytoskeleton in cultured renal proximal tubular cells (1986)
    Springer
    The journal of membrane biology 92 (1986), S. 151-162 
    Details
    ISSN: 1432-1424
    Keywords: kidney ; parathyroid hormone ; angiotensin II ; calcium ; brush border ; cytoskeleton
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary In order to examine the possibility of parathyroid hormone-mediated ultrastructural rearrangements in target epithelium, isolated canine renal proximal tubular cells were grown on a collagen-coated semipermeable membrane in a defined medium. Scanning and transmission electron microscopy of these monolayers revealed abundant microvilli. Exposure of the proximal tubular cells to parathyroid hormone resulted in a biphasic changes involving: (1) dramatic shortening and rarefaction of microvilli within 1 min; and (2) recovery of microvillar topography after 5 min. A similar shortening of microvilli was observed following exposure to ionomycin, whereas incubation with cyclic AMP resulted in an elongation of microvilli. Parathyroid hormone stimulated cyclic AMP production and increased cytoplasmic free calcium concentration in cultured proximal tubular cells. Pretreatment of cells with a calmodulin inhibitor abolished the effect of parathyroid hormone on brush border topography. Shortening of microvilli was associated with a disappearance of microvillar core filaments. Staining of F-actin with fluoresceinphalloidin showed that parathyroid hormone resulted in fragmentation of stress fibers. It is concluded that parathyroid hormoneinduced cell activation involves cytoplasmic-free calcium, calmodulin, and the cytoskeleton.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01870704
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  • 3
    Electronic Resource
    Electronic Resource
    THERAPEUTIC EFFECT OF ARGININE–GLYCINE–ASPARTIC ACID PEPTIDES IN ACUTE RENAL INJURY (1998)
    Melbourne, Australia : Blackwell Science Asia Pty. Ltd.
    Clinical and experimental pharmacology and physiology 25 (1998), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Previous studies from our laboratory have suggested that arginine–glycine–aspartic acid (RGD) peptides, serving as a decoy, may prevent tubular obstruction in the ischaemic model of acute renal failure. Specifically, we have demonstrated that: (i) stressed tubular epithelial cells reverse the polarity of integrin receptors from the predominantly basolateral location to the apical cell membrane as a part of a more generalized process of the loss of epithelial cell polarity; (ii) depletion of integrins expressed on the basal cell surface leads to the loss of anchorage to the basement membrane and cell desquamation; (iii) expression of integrin receptors on the apical cell membrane leads to indiscriminate interactions (e.g. the adhesion of desquamated cells to the cells remaining in situ), thus initiating the process of tubular obstruction; and (iv) conglomeration of the desquamated cells via integrin receptors further aggravates tubular obstruction.2. Importantly, these integrin-based interactions can be blocked by synthetic RGD peptides. The linear RGD peptide injected into the renal artery upon release of the renal artery clamp prevented the elevation of proximal tubular hydrostatic pressure characteristically seen in animals with renal ischaemia that received injection of the vehicle of an inactive peptide.3. In vivo study of RGD peptides in ischaemic acute renal failure in rats demonstrated attenuation of renal injury and accelerated recovery of renal function.4. Using linear RGD peptide labelled with 99mTc, we have shown that this probe was retained in ischaemic kidneys.5. To visualize RGD binding sites at the cellular level, we performed a mapping using fluorescent derivatives of two RGD peptides, a cyclic biotinylated (Bt)-RGD peptide and a linear Rhodamine green-labelled (RhoG)-RGD peptide.6. The findings suggest that the binding sites for RGD peptide are represented by the αVβ3 integrin in the vasculature and some desquamated cells, whereas the majority of the desquamated cells bind Bt-RGD via β1 integrins.7. These findings were further tested using cultured endothelial cells co-incubated with leucocytes. When co-incubation experiments were performed in the presence of cyclic RGD pentapeptide, the adhesion of HL-60 cells to both control and hypoxic endothelial monolayers was significantly reduced.Presented at the Experimental Biology Symposium on the Role of Integrins in Acute Renal Failure, New Orleans, Louisiana, USA, 1997.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1998.t01-2-.x
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  • 4
    Electronic Resource
    Electronic Resource
    CO-OPERATION BETWEEN ENDOTHELIN AND NITRIC OXIDE IN PROMOTING ENDOTHELIAL CELL MIGRATION AND ANGIOGENESIS (1999)
    Melbourne, Australia : Blackwell Science Pty
    Clinical and experimental pharmacology and physiology 26 (1999), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Among the diverse functions of endothelins (ET), their role in the remodelling of blood vessels remains poorly examined. In the present review, we summarize findings obtained in our laboratory and present four independent lines of evidence to support this novel function. We also demonstrate that the motogenic and angiogenic effects of ET are mediated via the ETB receptor and that the functional endothelial nitric oxide synthase (NOS) is requisite for this action.2. We demonstrated that ET stimulates transmigration of endothelial cells in a modified Boyden chamber and accelerates endothelial wound healing acting via ETB receptors.3. In genetically engineered Chinese hamster ovary cells expressing either ETB receptor or endothelial NOS or both, application of ET results in accelerated cell migration only when the receptor and the enzyme are coexpressed. Application of antisense oligonucleotides producing a specific knockdown of the endothelial NOS results in the loss of ET ability to stimulate endothelial cell migration in response to ET.4. Finally, using a novel model of in vivo angiogenesis, we were able to demonstrate that ET enhances formation of new vessels, but this effect requires functional endothelial NOS.5. The described phenomenon of NO production, serving as a prerequisite for endothelial cell locomotion in response to activation of ETB receptor may explain a host of pathophysiological observations on inadequate angiogenesis despite enhanced generation of ET-1.6. Based on the contribution of endothelial cell migration to angiogenesis, these data may implicate insufficient NO production in pathological states (e.g. atherosclerosis, heart failure and hypertension) in the inappropriate response to angiogenic stimuli.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1681.1999.03029.x
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  • 5
    Electronic Resource
    Electronic Resource
    ROLE OF MESANGIAL CELLS IN MACULA DENSA TO AFFERENT ARTERIOLE INFORMATION TRANSFER (1997)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 24 (1997), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Extraglomerular mesangial cells are strategically positioned between the macula densa and the afferent arteriole. These cells form a syncytium and are connected with glomerular mesangial cells via gap junctions. The model of immunoablation of mesangial cells in anti-Thy-1 glomerulonephritis carries the promise for understanding the function of mesangial cells as potential transmitters of information between the macula densa and the afferent arteriole.2. The above anatomical relations between structures in the juxtaglomerular apparatus predict several possible routes of information flow. This review charts some hypothetical routes.3. Research into the messenger systems involved in the transfer of signals from the macula densa to mesangial cells and from mesangial cells to the afferent arteriole suggests several candidate molecules to function in this capacity. Mechanisms of action for each candidate are discussed.4. The oscillating nature of the afferent signal and efferent function in the tubuloglomerular feedback system, as well as other discoveries, offer a fertile field for future studies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1997.tb01240.x
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  • 6
    Electronic Resource
    Electronic Resource
    Effects of Phorbol Ester, Cyclic Nucleotides, and Ionomycin on Ion Transport and Brush-Border Topography in Cultured Renal Proximal Tubular Cells (1987)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 494 (1987), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1987.tb29525.x
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  • 7
    Electronic Resource
    Electronic Resource
    Angiotensin-II stimulates nitric oxide release in isolated perfused renal resistance arteries (1998)
    Springer
    Pflügers Archiv 435 (1998), S. 432-434 
    Details
    ISSN: 1432-2013
    Keywords: Key words Kidney ; Losartan ; Candesartan ; NO-sensitive electrode
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Nitric oxide (NO) has been implicated as a modulator of the vascular effects of angiotensin II (ANG II) in the kidney. We used a NO-sensitive microelectrode to study the effect of ANG II on NO release, and to determine the effect of selective inhibition of the ANG II subtype I receptor (AT1) with losartan (LOS) and candesartan (CAN). NO release from isolated and perfused renal resistance arteries was measured with a porphyrin-electroplated, carbon fiber. The vessels were microdissected from isolated perfused rat kidneys and perfused at constant flow and pressure in vitro. The NO-electrode was placed inside the glass collection cannula to measure vessel effluent NO concentration. ANG II stimulated NO release in a dose-dependent fashion: 0.1 nM, 10 nM and 1000 nM ANG II increased NO-oxidation current by 85±18 pA (n = 11), 148±22 pA (n = 11), and 193±29 pA (n = 11), respectively. These currents correspond to changes in effluent NO concentration of 3.4±0.5 nM, 6.1±1.1 nM, and 8.2±1.3 nM, respectively. Neither LOS (1 μM) nor CAN (1 nM) significantly affected basal NO production, but both AT1-receptor blockers markedly blunted NO release in response to ANG II (10 nM): 77±6% inhibition with LOS (n = 8) and 63±9% with CAN (n = 8). These results are the first to demonstrate that ANG II stimulates NO release in isolated renal resistance arteries, and that ANG II-induced NO release is blunted by simultaneous AT1-receptor blockade. Our findings suggest that endothelium-dependent modulation of ANG II-induced vasoconstriction in renal resistance arteries is mediated, at least in part, by AT1-receptor-dependent NO release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050535
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  • 8
    Electronic Resource
    Electronic Resource
    Termination of endothelin signaling: Role of nitric oxide (1994)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 158 (1994), S. 485-494 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Cellular mechanisms responsible for the termination of ET-1 signal are poorly understood. In order to examine the hypothesis that nitric oxide serves as a physiological brake of ET- 1 signaling, Chinese hamster ovary (CHO) cells stably transfected with the ETA receptor cDNA (CHO-ET) were studied. CHO-ET responded to ET-1 with robust [Ca2+], transients and developed a long-lasting homologous desensitization. Donors of nitric oxide (NO), 3-morpholino-sydnonimine HCl(SIN-1), or sodium nitroprusside (SNP) reduced the amplitude of these responses, accelerated the rate of [Ca2+], recovery, and counteracted the development of homologous desensitization by a cyclic GMP-independent mechanism, suggesting an alternative mode for NO modulation of ET-1 responses. Stimulation of CHO-ET cells with mastoparan, a wasp venom acting directly on G proteins (bypassing receptor activation), was inhibited by NO, revealing a postreceptoral target for NO-induced modulation of [Ca2+] mobilization. Using a lys9-biotinylated ET-1 (ET-1 [BtK9]), binding sites were “mapped” in CHO-ET cells. Receptor-ligand complexes did not exhibit spontaneous dissociation during 60min observations. Quantitative fluorescence microscopy revealed that SNP or SIN-1 caused a rapid, concentration-dependent, and reversible dissociation of biotinylated ET- 1 from ETA receptor (EC50 = 75 μM and 6 μM, respectively), an effect that was not mimicked by 8-bromo-cyclic GMP. “Sandwich” co-culture of endothelial cells with CHO-ET showed that activation of NO production by endothelial cells similarly resulted in dissociation of ET-1 [BtK9] from ETA receptors. We hypothesize that NO plays a role in physiological termination of ET-1 signalling by dual mechanisms: (1) displacement of bound ET-1 from its receptor, thus preventing homologous desensitization, and (2) interference with the postreceptoral pathway for [Ca2+] mobilization, hence inhibiting end-responses to ET-1. © 1994 Wiley-Liss, Inc.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041580313
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  • 9
    Electronic Resource
    Electronic Resource
    Alpha1-adrenergic stimulation and cytoplasmic free calcium concentration in cultured renal proximal tubular cells: Evidence for compartmentalization of quin-2 and fura-2 (1986)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 128 (1986), S. 466-474 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: This study was designed to examine the role of changes in cytoplasmic free calcium concentration ([Ca2+]i) during the response to α1-adrenergic agonists in cultured renal proximal tubular cells. Experiments were carried out on primary cultures of canine proximal tubular cells grown in defined culture medium on a solid support, on collagen-coated polycarbonate membranes, or on collagen-coated glass coverslips. Quin-2 and fura-2 were used to monitor [Ca2+]i. The basal level of [Ca2+]i was 101 nM, as measured with quin-2, and 122 nM, as determined using fura-2. Fluorescence flow cytometry revealed that about 85% of the population of proximal tubular cells responded to phenylephrine with an increase in [Ca2+]i. Phenylephrine (10-5 M) caused an immediate actual increase in [Ca2+]i by 18 and 24%, as determined with quin-2 and fura-2, respectively, with the peak increase in [Ca2+]i averaging 22% and 44% over the basal level (180-300 sec). This effect did not require extracellular calcium. The effect of phenylephrine was abolished by prazosin and verapamil. Fluorescence microscopy of quin-2 or fura-2 loaded cells revealed punctate areas of fluorescence within the cytoplasm suggesting vesicular uptake of the dyes. Pinocytotic entrapment of the dyes was demonstrated by the transfer of cell-impermeant fura-2 across tubular cell monolayers mounted in Ussing chambers. The transfer of the dye was similar to that of a marker of fluid-phase pinocytosis, Lucifer Yellow (LY). This pinocytotic entrapment of Ca2+-indicators would lead to underestimation of the actual calcium transients. Microfluorometric study of single proximal tubular cells “scrape-loaded” with fura-2 revealed a four-fold increase in [Ca2+]i concentration following stimulation with phenylephrine.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041280316
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