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1.
Glycosylation defects alter insulin but not insulin-like growth factor I binding to Chinese hamster ovary cells 总被引:2,自引:0,他引:2
J M Podskalny D G Rouiller G Grunberger R C Baxter A McElduff P Gorden 《The Journal of biological chemistry》1986,261(30):14076-14081
Insulin binding to two Chinese hamster ovary cell lines with well-defined defects in their glycosylation pathway has been characterized and compared to insulin-like growth factor I (IGF-I) binding in the same cell lines. Insulin competition curves indicate that B4-2-1 cells, which transfer co-translationally to proteins an endoglycosidase H insensitive, truncated lipid-linked oligosaccharide, bind insulin with higher than normal affinity. Lec 1 cells, which fail to process oligosaccharide side chains to complex types, bind with a reduced affinity. The potencies of chicken and guinea pig insulins are appropriate for an insulin receptor in the control (WTB) and both mutant cell lines, whereas rat IGF-II is 3 times more potent than expected in the Lec 1 cells and human IGF-I is less potent than anticipated. Insulin bound to Lec 1 cells dissociates more quickly upon dilution than does insulin bound to either WTB or B4-2-1 cells. The Lec 1 insulin receptor is insensitive to pH change, whereas the other lines show the usual optimum of 8. 125I-IGF-I binds well to all three cell lines and is equally pH-sensitive in all three. Serum from a patient with circulating autoantibodies to the insulin receptor competes for insulin but not IGF-I binding, whereas alpha IR3, a monoclonal antibody directed toward the human IGF-I receptor inhibits IGF-I but not insulin binding. Cross-linking of either 125I-insulin or 125I-IGF-I reveals a typical alpha-subunit in the WTB and B4-2-1 cells but a band with faster mobility in the Lec 1 cells. Insulin (10(-8) M) stimulates autophosphorylation of a beta-subunit in all three lines, but again the Lec 1 subunit demonstrates an anomalous mobility on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. These data demonstrate the differential effect of glycosylation on two closely related receptor molecules. 相似文献
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Summary Zymosan given to rats, normal or splenectomized, stimulates the RES of the liver. Under this stimulation, the endothelial cells of the sinusoids change into Kupffer cells. The endothelial cells become hypertrophic and multiply; they acquire progressively the properties of phagocytosis and of digestion shown by the Kupffer cells. Hence both types of cells — the endothelial and the Kupffer cells — belong to the same cellular lineage. Their various aspects result from different functional states.The hyperplasia of the liver RES has no repercussion on the fine structure of the hepatic cells.
Mit Unterstützung durch den Schweizerischen Nationalfond für die Förderung der Wissenschaftlichen Forschung.
Stipendiat der Organisation Mondiale de la Santé.Übersetzung von Frau Antje Forssmann, technische Mitarbeit von Max Baumann, Michel Bernard und Charles Moreillon. 相似文献
Résumé L'administration de Zymosan à des rats, splénectomisés ou non, provoque une stimulation du SRE du foie. Sous l'effet de cette stimulation, les cellules endothéliales des sinusoïdes se transforment en cellules de Kupffer. Les cellules endothéliales s'hypertrophient et se multiplient; progressivement, elles acquiérent les propriétés de phagocytose et de digestion des cellules de Kupffer. Les deux types de cellules — endothéliales et cellules de Kupffer — appartiennent donc bien à la même lignée cellulaire. Leurs divers aspects correspondent à des états fonctionnels différents.L'hyperplasie du SRE du foie n'a pas de répercussion sur l'ultrastructure des hépatocytes.
Mit Unterstützung durch den Schweizerischen Nationalfond für die Förderung der Wissenschaftlichen Forschung.
Stipendiat der Organisation Mondiale de la Santé.Übersetzung von Frau Antje Forssmann, technische Mitarbeit von Max Baumann, Michel Bernard und Charles Moreillon. 相似文献
6.
Thierry Becquer Denis Merlet Jean-Pierre Boudot James Rouiller Francis Gras 《Plant and Soil》1990,125(1):95-107
Nitrate uptake and leaching were measured during one year in a declined fir forest on the Vosges highlands (eastern France),
in order to investigate whether excess nitrification could be responsible for a deleterious acidification of the ecosystem.
Nitrate uptake by the vegetation was active mainly from spring to early fall, and then reached about 66 kg N ha-1. No significant leaching loss occurred during the growth period of the vegetation. Significant nitrate leaching occurred
in winter (about 17 kg N ha-1). During fall and winter the nitrification rate was of the same magnitude as values reported for other ecosystems, and, thus,
was not considered to be abnormaly strong. No abnormal temporal discoupling of nitrate production and nitrate uptake occurred
in the ecosystem, and forest decline must therefore have some other cause. 相似文献
7.
Effect of bombesin upon plasma somatostatin-like immunoreactivity, insulin and glucagon in normal and chemically sympathectomized dogs 总被引:2,自引:0,他引:2
The present study was designed to determine the effects of intravenously infused bombesin (10 ng/kg/min) upon basal and postprandial plasma somatostatin-like immunoreactivity (SLI), glucagon, insulin and triglyceride levels in normal (n = 12) and chemically sympathectomized (n = 11) dogs. Basal plasma SLI, glucagon and insulin levels rose significantly during the infusion of bombesin in the normal dogs, and this was not altered by chemical sympathectomy. Bombesin infusion enhanced the postprandial SLI response, while attenuating the postprandial glucagon response by 50% and the insulin response in the early postprandial phase of the meal. Sympathectomy did not significantly alter the basal levels of these polypeptides, but augmented the postprandial plasma SLI response during the first 90 min, and reduced the postprandial glucagon response during the infusion of bombesin. The postprandial insulin response was not affected by sympathectomy. In both normal and chemically sympathectomized dogs the rise in postprandial triglyceride levels was attenuated by bombesin infusion. 相似文献
8.
Rat islets of Langerhans are organized as a core of B-cells surrounded by non-B-cells. It is believed that cell type segregation during histogenesis is the result of the differential expression of cell adhesion molecules (CAMs). Since we have previously shown that in contrast to non-B-cells, homotypic adhesion of pancreatic B-cells is dependent on the presence of Ca2+, the possibility exists that Ca(2+)-dependent CAMs (cadherins) might be in part responsible for islet topography. We now demonstrate that after selective removal of Ca(2+)-independent CAMs from the surface of islet cells by mild trypsin/Ca2+ digestion (TC-treatment), there is no significant difference in homotypic adhesion between sorted B- and non-B-cells in the presence of calcium, suggesting an identical deployment of cadherins. Flow cytometric analysis reveals high levels of uvomorulin on both B- and non-B-cells, without any difference between the two populations. On a "1 to 100" scale, B-cell aggregation in the presence of Ca2+ was decreased by anti-uvomorulin Fab fragments from 67 +/- 4 to 25 +/- 3 (mean +/- SEM, n = 4, P less than 0.01). This level is not different from the degree of B-cell aggregation seen in the presence of 0.5 mM EDTA (22 +/- 2). Aggregation of non-B-cells was only slightly decreased by anti-uvomorulin Fab fragments (from 69 +/- 3 to 52 +/- 4). However, after TC-treatment, homotypic cell aggregation of both B- and non-B-cells was completely inhibited by anti-uvomorulin Fab fragments. Thus, uvomorulin appears to be the only functional cadherin on islet cells, and cell type aggregation properties diverge only by virtue of higher levels of Ca(2+)-independent CAMs on non-B-cells. Fab fragments with the property of perturbing islet cell aggregation in the absence but not in the presence of calcium also prevented pseudoislet organization in vitro, suggesting that Ca(2+)-independent CAMs play the major role in islet cell type segregation. In conclusion, the results show that uvomorulin is responsible for the Ca(2+)-dependent aggregation of islet cells and suggest that the cellular organization within islets or pseudoislets results from the different level of Ca(2+)-independent CAMs on islet cell types. 相似文献
9.
Infusion of prostaglandin E2 (1 ug/kg/min) in six normal dogs elicited a greater than two-fold rise in pancreaticoduodenal vein somatostatin-like immunoreactivity. Insulin and glucagon also rose. The results raise the possibility that the function of the canine pancreatic D-cell is under prostaglandinergic influence. 相似文献
10.
J M Podskalny D G Rouiller A McElduff P Gorden 《Biochemical and biophysical research communications》1986,140(3):821-826
The pattern of cellular protein glycosylation can be altered in CHO cells by glucose starvation. When wild type CHO cells are deprived of glucose, 125I-insulin binding increases from a B/F of 0.033 +/- 0.004 to 0.063 +/- 0.011, due to an increase in receptor affinity. The already elevated insulin binding to mutant B4-2-1 CHO cells, whose genetic defect causes abnormal glycosylation mimicking the pattern seen in the glucose starved normal cells, is not affected by glucose starvation. In neither cell line is 125I-IGF-I binding affected by glucose starvation. These data support the hypothesis that abnormal glycosylation can alter insulin binding to its receptor. Furthermore, there is a striking difference in the susceptibility of IGF-I and insulin receptors to alterations in glycosylation. 相似文献