Glucose Inhibits Prostacyclin Production by Cultured Aortic Endothelial Cells

Hiroshi Ono; Fumio Umeda; Toyoshi Inoguchi; Hiroshi Ibayashi

doi:10.1055/s-0038-1647024

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 1988; 60(02): 174-177
DOI: 10.1055/s-0038-1647024

Original Article

Schattauer GmbH Stuttgart

Glucose Inhibits Prostacyclin Production by Cultured Aortic Endothelial Cells

Authors

Hiroshi Ono

The Third Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan
Fumio Umeda

The Third Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan
Toyoshi Inoguchi

The Third Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan
Hiroshi Ibayashi

The Third Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan

Abstract

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Summary

A reduction in production of prostacyclin (PGI₂) by the cells in the vascular wall may play a role in the pathogenesis of atherosclerosis in diabetic patients. The present study was undertaken to evaluate the effect of glucose on PGI₂ production by endothelial cells in vitro. It was shown that PGI₂ production by cultured bovine aortic endothelial cells was significantly reduced in the presence of a high concentration of glucose (300 mg/dl) compared with physiological concentrations of glucose (100 mg/ dl). In contrast, no reduction in PGI₂ production was observed in cells cultured with equimolar mannitol, suggesting that glucose itself, rather than the effect of osmolality, inhibited PGI₂ production by cultured endothelial cells.

In addition, a high concentration of glucose also inhibited the proliferation of cultured endothelial cells.

Keywords

Glucose - Prostacyclin - Vascular endothelial cells Summary

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References

References
1 Robertson WB, Strong JR. Atherosclerosis in persons with hypertension and diabetes. Lab Invest 1968; 18: 538-551
2 Crall FV, Roberts WC. The extramural and intramural coronary arteries in juvenile diabetes mellitus. Am J Med 1978; 64: 221-230
3 Colwell JA, Lopes-Virella ML, Halushka PV. Pathogenesis of atherosclerosis in diabetes mellitus. Diabetes Care 1981; 4: 121-133
4 Colwell JA, Winocour PD, Lopes-Virella M, Halushka PV. New concepts about the pathogenesis of atherosclerosis in diabetes mellitus. Am J Med. 1983. Suppl 67-80
5 Moncada S, Gryglewski R, Bunting S, Vane JR. An enzyme isolated from arteries transforms prostaglandin endoperoxides to an unstable substance that inhibits platelet aggregation. Nature 1976; 263: 663-665
6 Moncada S, Vane JR. Unstable metabolites of arachidonic acid and their role in haemostasis and thrombosis. Br Med Bull 1978; 34: 129-135
7 Maclyntyre DE, Pearson JD, Gordon JL. Localisation and stimulation of prostacyclin production in vascular cells. Nature 1978; 271: 549-551
8 Weksler BB. Prostacyclin. Prog Hemostasis Thromb 1982; 6: 113-138
9 Johnson M, Harrison HE, Raftery AT, Elder JB. Vascular prostacyclin may be reduced in diabetes in man. Lancet 1979; 1: 325-326
10 Silberbauer K, Schernthaner G, Sinzinger H, Piza-Katzer H, Winter M. Decreased vascular prostacyclin in juvenile-onset diabetes. N Engl J Med 1979; 300: 366-367
11 Harrison HE, Reece AH, Johnson M. Decreased vascular prostacyclin in experimental diabetes. Life Sci 1978; 23: 351-356
12 Jeremy JY, Thompson CS, Mikhailidis DP, Dandona P. Experimental diabetes mellitus inhibits prostacyclin synthesis by the rat penis: pathological implications. Diabetologia 1985; 28: 365-368
13 Watanabe J, Umeda F, Inoguchi T, Wasada T, Ibayashi H. Decreased prostacyclin production and platelet abnormalities in diabetes mellitus (English abstract). J Jpn Diab Soc 1985; 28: 1229-1234
14 Subbiah MT R, Deitemeyer D. Altered synthesis of prostaglandins in platelet and aorta from spontaneously diabetic Wistar rats. Biochem Med 1980; 23: 231-235
15 Valentovic MA, Lubawy WC. Elevated glucose in vivo and in vitro adversely alters prostaglandins generation in rat aortas and platelets. Prost Leuk Med 1985; 19: 271-277
16 Inoguchi T, Umeda F, Watanabe J, Ibayashi H. Reduced serum stimulatory activity on prostacyclin production by cultured aortic endothelial cells. Haemostasis 1986; 16: 447-452
17 Umeda F, Franks DJ, Sugimoto H, Halle JP, Hamet P. Effect of plasma, serum and platelets from diabetics on DNA synthesis in cultured vascular smooth muscle cells. Clin Invest Med 1985; 8: 35-40
18 Hamet P, Sugimoto H, Umeda F, Lecavalier L, Franks DJ, Orth DN, Chiasson JL. Abnormalities of platelet-derived growth factors in insulin-dependent diabetes. Metabolism 1985; 34 suppl (Suppl. 01) 25-31
19 Franks DJ, Plamondon J, Hamet P. An increase in adenylate cyclase activity precedes DNA synthesis in cultured vascular smooth muscle cells. J Cell Physiol 1984; 119: 41-45
20 Lowry OH, Rosebrough NJ, Farr AL, Randall RJ. Protein measurement with the Folin phenol reagent. J Biol Chem 1957; 193: 265-275
21 Aanderud S, Krane H, Nordøy A. Influence of glucose, insulin and sera from diabetic patients on the prostacyclin synthesis in vitro in cultured human endothelial cells. Diabetologia 1985; 28: 641-644
22 Paton RC, Guillot R, Passa Ph, Canivet J. Prostacyclin production by human endothelial cells cultured in diabetic serum. Diabetes Metab 1982; 8: 323-328
23 Harrison HE, Reece AH, Johnson M. Effect of insulin treatment on prostacyclin in experimental diabetes. Diabetologia 1980; 18: 65-68
24 Stout RW. Glucose inhibits replication of cultured human endothelial cells. Diabetologia 1982; 23: 436-439
25 Lorenzi M, Cagliero E, Toledo S. Glucose toxicity for human endothelial cells in culture: delayed replication, disturbed cell cycle, and accelerated death. Diabetes 1985; 34: 621-627
26 Lorenzi M, Montisano DF, Toledo S, Barrieux A. High glucose induces DNA damage in cultured human endothelial cells. J Clin Invest 1986; 77: 322-325
27 Lorenzi M, Nordberg JA, Toledo S. High glucose prolongs cell-cycle traversal of cultured human endothelial cells. Diabetes 1987; 36: 1261-1267
28 Ross R. The pathogenesis of atherosclerosis: an update. N Engl J Med 1986; 314: 488-500