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  • 1990-1994  (4)
  • cultured rabbit gastric cells  (2)
  • protein kinase C  (2)
  • Pancreatic exocrine cell antibodies  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Translocation of protein kinase C α and ζ in rat glomerular mesangial cells cultured under high glucose conditions (1994)
    Springer
    Diabetologia 37 (1994), S. 838-841 
    Details
    ISSN: 1432-0428
    Keywords: Diabetic nephropathy ; glomerular mesangial cells ; protein kinase C ; isoenzymes ; high glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The activities and expression of protein kinase C isoenzymes were examined in glomerular mesangial cells cultured under high glucose conditions. Exposure of cells to high glucose concentrations (27.8 mmol/l) for more than 3 days resulted in a significant elevation of protein kinase C activities in the membrane fraction. Of the protein kinase C isoenzymes, the levels of protein kinase C α significantly increased in the membrane fraction after 3 days of exposure to glucose, and protein kinase C ζ increased after 5 days of exposure. Levels of protein kinase C δ and ε remained unchanged and protein kinase C Β and γ were not detected. These results indicate that protein kinase C α and ζ are translocated under high glucose conditions possibly through different mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404342
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Pancreatic cytokeratin: an antigen of pancreatic exocrine cell autoantibodies in Type 1 (insulin-dependent) diabetes mellitus (1990)
    Springer
    Diabetologia 33 (1990), S. 363-370 
    Details
    ISSN: 1432-0428
    Keywords: Pancreatic exocrine cell antibodies ; cytokeratin ; Type 1 (insulin-dependent) diabetes mellitus ; islet cell antibodies ; pancreatic exocrine cells ; pancreatic islet
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Autoantibodies reacting with human pancreatic exocrine cells were investigated by immunofluorescent techniques in 107 patients with Type 1 (insulin-dependent) diabetes mellitus, 20 first-degree relatives of the Type 1 diabetic patients, 347 patients with Type 2 (non-insulin-dependent) diabetes, 34 with alcoholic pancreatitis, 26 with rheumatoid arthritis and 107 normal control subjects. Both immunoblotting analysis and double-immunostaining methods were used to characterize the antigens targeted by the pancreatic exocrine cell autoantibodies. Sera positive for human pancreatic exocrine cell cytoplasm, producing a “fine fibrillar” pattern, were found in 21% (23/107) of the Type 1 diabetic patients. The autoantibodies were present in 39% (15/38) of Type 1 diabetic patients diagnosed within 3 months, and the prevalence decreased with duration of diabetes. The antibodies were of the IgM class in 87% (13/15) of recent-onset Type 1 diabetes cases, but IgG-autoantibodies became more prevalent with increasing duration of diabetes. Three out of 347 (0.9%) Type 2 diabetic patients and 4 of 20 (20%) first-degree relatives of Type 1 diabetic patients had autoantibodies targeted against pancreatic exocrine cells. None of the patients with alcoholic pancreatitis or rheumatoid arthritis and none of the control subjects had these antibodies. Immunoblotting analysis and double-immunostaining demonstrated that the autoantibodies reacted with 40 kilodalton cytokeratin in pancreatic exocrine cell cytoplasm. The antibody was absorbed by the Triton X-100-insoluble fraction of pancreatic extract. These results indicate the presence of distinct autoantibodies to pancreatic exocrine cells in Type 1 diabetes. This suggests the provocative concept that the cytoskeletal system of pancreatic exocrine cells is involved in the pathogenetic process of Type 1 diabetes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404641
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Roles of Ca2+ and protein kinase C in regulation of prostaglandin E2 release by cultured rabbit gastric epithelial cells (1993)
    Springer
    Digestive diseases and sciences 38 (1993), S. 1426-1434 
    Details
    ISSN: 1573-2568
    Keywords: cultured rabbit gastric cells ; prostaglandin E2 release ; protein kinase C ; Ca2+ ; cAMP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Prostaglandin (PG) has been reported to be one of the important protective factors in the gastric mucosa. However the mechanism of the regulation of endogenous PG production has not been well studied. We investigated the possible roles of Ca2+, cAMP, and protein kinase C (PKC) in the regulation of PGE2 release from cultured rabbit gastric mucosal cells. PGE2 was measured by radioimmunoassay. A23187 (Ca2+ ionophore) at 2×10−6 M significantly increased PGE2 release. Deprivation of Ca2+ from the medium blocked the A23187-induced increase of PGE2. TMB-8 (a putative inhibitor of Ca2+ release from intracellular stores) did not have any significant effects on the increase of PGE2-induced by A23187. Thus, A23187 increased PGE2 through the influx of extracellular Ca2+. W7 or compound 48/80 (calmodulin inhibitors) did not alter the response of PGE2 caused by A23187. Exogenous administration of cAMP, forskolin (an activator of adenylate cyclase), or 2-chloroadenosine (a possible activator of adenylate cyclase through adenosine A2 receptor) had neither significant effects on PGE2 release nor an effect on A23187-induced increase of PGE2 release. 12-O-tetradecanoylphorbol 13-acetate (TPA, an activator of PKC) significantly stimulated PGE2 release in a dose-dependent fashion, whereas another phorbol ester with no biological activity did not. A23187 at 0.8×10−6 M, but not cAMP, potentiated the TPA-induced increase of PGE2. Mepacrine (a phospholipase A2 inhibitor) reduced the A23187-and TPA-induced increase of PGE2. These results suggest that Ca2+ and protein kinase C may play important roles in the regulation of PGE2 release by cultured rabbit gastric cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01308599
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Protective effect of tauroursodeoxycholate against chenodeoxycholate-induced damage to cultured rabbit gastric cells (1991)
    Springer
    Digestive diseases and sciences 36 (1991), S. 409-416 
    Details
    ISSN: 1573-2568
    Keywords: cultured rabbit gastric cells ; cytoprotection ; tauroursodeoxycholate ; ursodeoxycholate ; chenodeoxycholate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Ursodeoxycholate (UDC) and tauroursodeoxycholate (TUDC) have been reported to be protective against liver injury induced by other bile salts. UDC also has been shown to be effective against refluxed bile-induced gastritis after gastric surgery. However the mechanism of the therapeutic effect of UDC on gastric mucosa has not been known. In the present study, cytoprotective actions of UDC and TUDC against chenodeoxycholate (CDC)-induced gastric injury were investigated using rabbit gastric cell cultures without systemic factors. Rabbit gastric mucosal cells were cultured after the isolation of rabbit gastric cells with collagenase and ethylenediaminetetraacetic acid. Cytotoxicity was quantified by measuring51Cr release from prelabeled cells and MTT assay. Prostaglandin (PG) E2 was assayed by radioimmunoassay. Concentrations of CDC〉0.5mM or UDC〉5mM caused cellular damage and increased51Cr release in a dose-dependent and time-dependent fashion, while TUDC up to 10 mM did not. TUDC, but not UDC, showed a significant decrease of CDC (1.5 mM)-induced51Cr release dose dependently. The protective effect of TUDC against CDC-induced damage was confirmed by MTT assay. On phase-contrast microscopy, disruption of monolayers induced by CDC (1.5 mM) was clearly protected by TUDC (10 mM). Free radical scavengers (500 units/ml of superoxide dismutase, 300 units/ml of catalase, and 100 mM of dimethyl sulfoxide) or a calcium blocker (10−7–10−5 M verapamil) did not show significant protection against CDC-induced damage. Deprivation of Ca2+ in the media did not affect CDC-induced damage. Thus free radicals of Ca2+ might not be involved in the cell toxicity of CDC. Although TUDC (10 mM) significantly increased PGE2 production by cultured cells, indomethacin (10−4 M) did not reduce protective effects of TUDC, as assessed by51Cr release and MTT assay. In conclusion TUDC is cytoprotective against CDC-induced damage to cultured rabbit gastric cells. Neither free radicals, Ca2+, nor endogenous PGs may play leading roles in the mechanism of this action.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01298867
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    Paper (German National Licenses)
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