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  • 1
    Electronic Resource
    Electronic Resource
    Morphine Stimulates Mesangial Cell TNF-α and Nitrite Production (2000)
    Springer
    Inflammation 24 (2000), S. 463-476 
    Details
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background: Intravenous opiate abusers are susceptible to develop heroin and HIV-associated nephropathies; however, the role of opiates in the development of these kidney lesions is not clear. Patients with opiate addiction are prone to recurrent infections. Methods: The effect of morphine was studied on the generation of TNF-α with or without LPS (lipopolysaccharide) by cultured mouse mesangial cells. In addition, the effect of morphine was evaluated on mesangial cell nitrite production. To evaluate the role of opiate receptors, we studied the effect of naloxone and naltrexone on mesangial cell TNF-α and nitrite production. To determine the role of TNF-α on mesangial cell nitrite production, we examined the effect of anti-TNF-α antibody on morphine-induced nitrite production. Assay of TNF-α and nitrite production was carried by ELISA and Griess method respectively. Results: Morphine alone did not enhance the generation of TNF-α by mesangial cells, however, an enhanced (P 〈 0.001) TNF-α production was observed when mesangial cells were first treated with morphine for 18 h and then activated further with LPS. Maximum release of TNF-α was seen at a concentration of 10−12 M of morphine. Opiate receptor antagonists (naloxone and naltrexone) inhibited the effect of morphine. Morphine also amplified (P 〈 0.0002) the effect of LPS on mesangial cell nitrite production. Anti-TNF-α antibody attenuated morphine induced nitrite generation. Conclusion: We conclude that morphine stimulates the generation of TNF-∝ by LPS-activated mesangial cells. This effect of morphine seems to be opiate receptor mediated and has a downstream effect in the form of mesangial cell nitrite generation. The present in vitro study provides the basis for a hypothesis that morphine may be playing a role in the development of heroin and HIV-associated nephropathies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007016329300
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  • 2
    Electronic Resource
    Electronic Resource
    Oxidation of the Mesangial Matrix Metalloproteinase-2 Impairs Gelatinolytic Activity (1998)
    Springer
    Inflammation 22 (1998), S. 269-276 
    Details
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Glomerulosclerosis is characterized by an accumulation of mesangial extracellular matrix. Oxygen radicals are strongly implicated in glomerular injury but it is unclear by what mechanism they could modulate matrix turnover dynamics. We evaluated whether oxidation of the 72 kD mesangial matrix metalloproteinase-2 (MMP-2), the major mesangial matrix-degrading enzyme, could alter its gelatinolytic activity. Oxidation of the MMP-2 using a FeCl3/ascorbate system resulted in impaired ability to degrade [3H]gelatin compared to control. Samples were also subjected to SDS-PAGE gelatin substrate zymography. At the 72 kD position a significant impairment of gelatinolytic activity of oxidized samples was observed, a decrease attenuated by coincubation of samples with the FeCl3/ascorbate system plus the radical spin trap N-tert-butyl-α-phenylnitrone suggesting specificity of oxidative changes in the decrease in enzymatic activity. These data represent the first report demonstrating that oxidation of the MMP-2 diminishes its activity and suggest a previously undescribed mechanism by which oxygen radicals may contribute to altered turnover of extracellular matrix.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1022396015294
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Macrophage supernatants have both stimulatory and suppressive effects on mesangial cell proliferation (1993)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 154 (1993), S. 289-293 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Macrophages may modulate mesangial expansion following renal injury via secretory products. We undertook the present study to determine the effects of macrophages supernatants on mesangial cell proliferation. Macrophage supernatants collected in serum-free media after 24 hours caused significantly enhanced mesangial cell proliferation in long-term culture at concentration up to 50% but caused suppression at higher concentration (control, 122,000 ± 14,000 cells/well: 50% supernatant, 188,000 ± 15,100 cells/well, p 〈 0.02 compared to control, n = 4; 80% supernatant, 52,000 ± 3,500 cells/well, P 〈 0.01 compared to control, n = 4). In short-term culture [3H] thymidine incorporation, a measure of DNA synthesis, was significantly enhanced compared to control at supernatant concentrations up to 30% (30% supernatant, 4,120 ± 310 cpm/well; control, 3,210 ± 97 cpm/well, P 〈 0.5, n = 4), but uptake was reduced at high concentration (80% supernatant, 2,900 ± 74 cpm/well; control, 3,210 ± 97 cpm/well, P 〈 0.05, n= 4) When macrophages supernatants were collected after 48 hours incubation and incubated with mesangial cells, mesangial cell thymidine uptake was significantly suppressed compared to control (48-hours supernatant, 4,060 ± 260 cpm/well; control, 5,890 ± 270 cpm/well, P 〈 0.01, n = 4) and comapared to 24-hour supernatants, which enhanced uptake (24-hour supernatant, 8,080 ± 340 cpm/well; control, 5,890 ± 270 cpm/well, P 〈 0.01, n =4). Our results suggest that macrophages supernatants can directly enhance mesangial cell proliferation in vitro in both short-term and long-term culture, though this effect is lost at high concentrations of supernatant. These data lend support to the potential role of the macrophage in mediating mesangial expansion following renal injury. © 1993 Wiley-Liss, Inc.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041540211
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Extracellular matrix modulates mesangial cell apoptosis and mRNA expression of cathepsin-B and tissue transglutaminase (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 68 (1998), S. 22-30 
    Details
    ISSN: 0730-2312
    Keywords: cathepsin-B ; tissue transglutaminase ; mesangial cell apoptosis ; mRNA expression ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Mesangial matrix is a dynamic structure which modulates mesangial cell function. Since accumulation of matrix precedes the development of focal glomerulosclerosis, we studied the effect of different matrices on mesangial cell (MC) apoptosis. Suspended mesangial cells became apoptotic in a time dependent manner. Collagen type III did not modulate MC apoptosis when compared to cells grown on plastic. MCs grown on Matrigel, collagen type I and IV showed an increased number of apoptotic cells when compared to MCs grown on plastic. DNA end-labeling further confirmed these observations. MCs grown on Matrigel showed enhanced (P 〈 0.05) mRNA expression for tissue transglutaminase (TTG) and cathepsin-B. Mesangial cells grown on Matrigel also showed enhanced expression of superoxide dismutase (SOD). We conclude that mesangial cells require attachment to the matrix for their survival and alteration of the quality of matrix modulates mesangial cell apoptosis. J. Cell. Biochem. 68:22-30, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
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    Paper (German National Licenses)
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