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  • type IV collagen  (3)
  • glomerulopathy  (2)
  • HL-60 cells  (1)
  • Na+-coupled glucose transporter  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Increased rat myocardial type VI collagen in diabetes mellitus and hypertension (1993)
    Springer
    Diabetologia 36 (1993), S. 93-98 
    Details
    ISSN: 1432-0428
    Keywords: Diabetes mellitus ; hypertension ; diabetic cardiomyopathy ; type VI collagen ; type IV collagen ; type I collagen ; laminin ; myosin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diabetic cardiomyopathy, a condition characterized by the accumulation of carbohydrate-containing material surrounding the myocardial small blood vessels, has been studied in alloxan-diabetic normotensive and hypertensive rats. Immunochemical techniques were used to monitor several extracellular matrix constituents present in extracts of cardiac tissue, namely types I, IV and VI collagen, laminin and fibronectin, as well as myosin. These studies have indicated that after induction of diabetes, type VI collagen but none of the other matrix components studied, was significantly increased (from 2.29±0.04 mg/g in normal to 2.85±0.18 mg/g in diabetic ventricles, p〈0.01). Hypertension, whether induced by the clipping of one renal artery or genetically determined (spontaneously hypertensive rats), resulted in a similar elevation in type VI collagen (2.71±0.12 mg/g, p〈0.005 compared to normal rats). In the presence of diabetes plus hypertension the effect was not additive, the type VI collagen level being 2.93±0.15 (p〈0.001 compared to normal rats). Basement membrane collagen (type IV) in the myocardium appeared to be unaffected by diabetes or hypertension and the myosin contents of the hearts of the four experimental groups were similar. Quantitative determinations indicate that compared to type IV collagen, laminin or fibronectin, type VI collagen represents the major periodic acid-Schiff-reactive extracellular constituent of the rat ventricle. Its preferential increase in the heart in diabetes may provide insight into the molecular mechanisms of the diabetic microvascular disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400687
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Glucose entry into rat mesangial cells is mediated by both Na+-coupled and facilitative transporters (1995)
    Springer
    Diabetologia 38 (1995), S. 291-297 
    Details
    ISSN: 1432-0428
    Keywords: Key words Na+-coupled glucose transporter ; facilitative glucose transporters ; mesangial cells ; glomerulopathy ; phlorizin.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Since previous studies from our laboratory have demonstrated that increased glucose consumption by cultured rat mesangial cells is accompanied by an accelerated production of type IV and type VI collagen, we have now examined the manner by which glucose is transported into these cells. A progressive stimulation of glucose uptake by the mesangial cells was observed with increasing concentrations of NaCl so that at 145 mmol/l about twice as much glucose entered the cells as in its absence (substituted by choline chloride). Moreover, since phlorizin inhibited the NaCl-promoted uptake of glucose and this salt was found to increase the accumulation of α-methylglucoside in a manner which could not be duplicated by KCl or mannitol, both Na+-coupled and facilitative glucose transporters appeared to be present in the cells. Km values of 1.93 mmol/l and 1.36 mmol/l were determined for the co-transport and facilitated transport pathways, respectively, with their Vmax being 29.5 and 18.0 nmol · mg protein− 1· h− 1. Both uptake activities were found to be down-regulated by exposure of the cells to high glucose and furthermore the Na+-dependent transport could no longer be detected after about 12 passages of the cells. Hybridization of mesangial cell mRNA with cDNA probes revealed transcripts for the Na+/glucose co-transporter as well as GLUT1 and to a lesser extent GLUT4. The identification of the co-transporter in these non-polarized cells is pertinent to an understanding of the intracellular signals which can lead to the development of the diabetic glomerular lesions; in the hyperglycaemic state this carrier provides an additional route for accelerated glucose entry and furthermore by the attendant increase in Na+ flux may bring about an alteration in the ionic composition of the cell. [Diabetologia (1995) 38: 291–297]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400633
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Effect of high glucose on formation of extracellular matrix components by cultured rat heart endothelial cells (1995)
    Springer
    Diabetologia 38 (1995), S. 430-436 
    Details
    ISSN: 1432-0428
    Keywords: Rat heart endothelial cells ; type VI collagen ; type IV collagen ; type I collagen ; fibronectin ; GLUT1 ; high glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In an attempt to define the basis for the microvascular changes observed in diabetic myocardium, a study was undertaken on the effect of elevated glucose on the synthesis by rat heart endothelial cells of the extracellular matrix components, types VI, IV and I collagen, as well as fibronectin. Confluent cultures of these cells, isolated by fluorescence-activated cell sorting after treatment with rhodamine-labelled acetylated low density lipoprotein, showed a three to fivefold enhancement in the synthesis of type VI collagen after exposure for 48 h to high glucose (20 to 30 mmol/l), as determined by immunoblot analysis. Increased production of type IV collagen and fibronectin was also observed, but the change was smaller and no effect on type I collagen was found. Measurement of mRNA levels by hybridization with cDNA probes indicated that 48-h exposure to high glucose significantly increased the level of transcripts for type VI and IV collagens but not for type I collagen. While glucose consumption by endothelial cells in high glucose doubled in the initial 24-h period, utilization returned to normal by 48 h, concomitant with a reduction in GLUT1 transcript levels, suggesting that signals for stimulation of collagen synthesis must be active during the initial period of exposure to elevated glucose levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00410280
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Effect of high glucose on formation of extracellular matrix components by cultured rat heart endothelial cells (1995)
    Springer
    Diabetologia 38 (1995), S. 430-436 
    Details
    ISSN: 1432-0428
    Keywords: Key words Rat heart endothelial cells ; type VI collagen ; type IV collagen ; type I collagen ; fibronectin ; GLUT1 ; high glucose.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In an attempt to define the basis for the microvascular changes observed in diabetic myocardium, a study was undertaken on the effect of elevated glucose on the synthesis by rat heart endothelial cells of the extracellular matrix components, types VI, IV and I collagen, as well as fibronectin. Confluent cultures of these cells, isolated by fluorescence-activated cell sorting after treatment with rhodamine-labelled acetylated low density lipoprotein, showed a three to fivefold enhancement in the synthesis of type VI collagen after exposure for 48 h to high glucose (20 to 30 mmol/l), as determined by immunoblot analysis. Increased production of type IV collagen and fibronectin was also observed, but the change was smaller and no effect on type I collagen was found. Measurement of mRNA levels by hybridization with cDNA probes indicated that 48-h exposure to high glucose significantly increased the level of transcripts for type VI and IV collagens but not for type I collagen. While glucose consumption by endothelial cells in high glucose doubled in the initial 24-h period, utilization returned to normal by 48 h, concomitant with a reduction in GLUT1 transcript levels, suggesting that signals for stimulation of collagen synthesis must be active during the initial period of exposure to elevated glucose levels. [Diabetologia (1995) 38: 430–436]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00410280
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Glucose entry into rat mesangial cells is mediated by both Na+-coupled and facilitative transporters (1995)
    Springer
    Diabetologia 38 (1995), S. 291-297 
    Details
    ISSN: 1432-0428
    Keywords: Na+-coupled glucose transporter ; facilitative glucose transporters ; mesangial cells ; glomerulopathy ; phlorizin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Since previous studies from our laboratory have demonstrated that increased glucose consumption by cultured rat mesangial cells is accompanied by an accelerated production of type IV and type VI collagen, we have now examined the manner by which glucose is transported into these cells. A progressive stimulation of glucose uptake by the mesangial cells was observed with increasing concentrations of NaCl so that at 145 mmol/l about twice as much glucose entered the cells as in its absence (substituted by choline chloride). Moreover, since phlorizin inhibited the NaCl-promoted uptake of glucose and this salt was found to increase the accumulation of α-methylglucoside in a manner which could not be duplicated by KCl or mannitol, both Na+-coupled and facilitative glucose transporters appeared to be present in the cells. Km values of 1.93 mmol/l and 1.36 mmol/l were determined for the co-transport and facilitated transport pathways, respectively, with their Vmax being 29.5 and 18.0 nmol·mg protein−1· h−1. Both uptake activities were found to be down-regulated by exposure of the cells to high glucose and furthermore the Na+-dependent transport could no longer be detected after about 12 passages of the cells. Hybridization of mesangial cell mRNA with cDNA probes revealed transcripts for the Na+/glucose co-transporter as well as GLUT1 and to a lesser extent GLUT4. The identification of the co-transporter in these non-polarized cells is pertinent to an understanding of the intracellular signals which can lead to the development of the diabetic glomerular lesions; in the hyperglycaemic state this carrier provides an additional route for accelerated glucose entry and furthermore by the attendant increase in Na+ flux may bring about an alteration in the ionic composition of the cell.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400633
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Alkylphosphocholines induce apoptosis in HL-60 and U-937 leukemic cells (1997)
    Springer
    Cancer chemotherapy and pharmacology 41 (1997), S. 210-216 
    Details
    ISSN: 1432-0843
    Keywords: Key words Alkylphosphocholines ; HL-60 cells ; U-937 cells ; K-562 cells ; Apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Alkylphosphocholines (APC) represent a new group of ether-lipid-related compounds with remarkable activity against transformed cells in vitro and good tolerability in vivo. Their mechanism of action remains unknown. The aim of the present study was to investigate the effects of a series of APC on three human leukemic cell lines: K-562, HL-60, and U-937. The tetrazolium dye-reduction (MTT) assay and cell counting were used to determine the cytotoxicity of the APC used. DNA gel electrophoresis and enzyme-linked immunosorbent assay (ELISA) detection of oligonucleosomes were performed to identify and quantify DNA fragmentation. Electron and phase-contrast microscopy were used to detect morphologic changes specific for programmed cell death. HL-60 and U-937 cells were found to be sensitive, but K-562 cells were relatively resistant to APC exposure. APC with long alkyl chains exerted stronger cytotoxicity than did those with short alkyl chains. DNA fragmentation was found after treatment with APC in HL-60 and U-937 cells but not in K-562 cells. In HL-60 cells the increase in mono- and oligonucleosome formation as measured by ELISA was correlated with the length of the alkyl chains at 14 h of exposure to APC but plateaued at 20 h. The morphologic alterations in HL-60 and U-937 cell lines, such as cell shrinkage, chromatin condensation, and formation of apoptotic bodies, confirmed the induction of apoptosis after APC exposure. It is concluded that programmed cell death plays an important role in the cytotoxicity of APC against certain human leukemic cell lines. The antineoplastic profiles of APC with long alkyl chains render them attractive for further therapeutic application.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002800050730
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    Paper (German National Licenses)
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