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Titolo:
ADENOSINE INHIBITORY EFFECT ON ENHANCED GROWTH OF AORTIC SMOOTH-MUSCLE CELLS FROM STREPTOZOTOCIN-INDUCED DIABETIC RATS
Autore:
PARESHERBUTE N; HILLAIREBUYS D; ETIENNE P; GROSS R; LOUBATIERESMARIANI MM; MONNIER L;
Indirizzi:
CHU LAPEYRONIE,SERV MALAD METAB,371 AVE DOYEN GASTON GIRAND F-34295 MONTPELLIER 5 FRANCE LAPEYRONIE HOSP,DEPT METAB F-34295 MONTPELLIER 5 FRANCE FAC MED MONTPELLIER,PHARMACOL LAB MONTPELLIER FRANCE
Titolo Testata:
British Journal of Pharmacology
fascicolo: 3, volume: 118, anno: 1996,
pagine: 783 - 789
SICI:
0007-1188(1996)118:3<783:AIEOEG>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
ADENYLATE-CYCLASE ACTIVITY; ISLET-ACTIVATING PROTEIN; RECEPTOR; PROLIFERATION; GI; VASODILATORS; HEPATOCYTES; EXPRESSION;
Keywords:
DIABETES; ATHEROSCLEROSIS; SMOOTH MUSCLE CELLS; PRIMARY CULTURE; ADENOSINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
35
Recensione:
Indirizzi per estratti:
Citazione:
N. Paresherbute et al., "ADENOSINE INHIBITORY EFFECT ON ENHANCED GROWTH OF AORTIC SMOOTH-MUSCLE CELLS FROM STREPTOZOTOCIN-INDUCED DIABETIC RATS", British Journal of Pharmacology, 118(3), 1996, pp. 783-789

Abstract

1 There is evidence to suggest that adenosine may regulate arterial smooth muscle cell (SMC) growth and proliferation, which is a key eventin atherogenesis. This regulation may be mediated via adenylate cyclase. As diabetes is a known risk factor for atherosclerosis, we investigated the growth of aortic SMC from diabetic rats in primary culture and their sensitivity to adenosine and to adenylate cyclase activity. 2Diabetes was induced with streptozotocin (STZ, 66 mg kg(-1), i.p. ) Aortic SMC primary cultures were prepared from STZ-diabetic and age-matched rats 5 weeks after the STZ injection. 3 SMC from STZ-diabetic ratsgrew faster and reached greater densities at confluence than those from non-diabetic animals. 4 Adenosine inhibited growth in both control and diabetic SMC. However, cells from STZ-diabetic rats were apparently more sensitive to adenosine. 5 Direct activation of adenylate cyclase by forskolin induced a dose-dependent growth inhibition, similar in both groups of cells. 6 Cholera toxin, an activator of stimulatory GTP-binding protein (G(s)), induced a similar growth inhibitory response in non-diabetic and diabetic SMC. Pertussis toxin (PTX), an inactivator of inhibitory GTP-binding protein (G(i)), did not itself affect SMC growth. However, PTX increased dose-dependently the growth inhibition induced by adenosine in SMC from non-diabetic rats but not in SMC fromdiabetic rats. 7 These findings suggest a functional abnormality in G(i) activity in SMC from diabetic rats, that would explain the increased sensitivity to the nucleoside. This impaired inhibitory pathway mayreflect changes in the growth regulation of SMC in experimental diabetic states.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 09:31:53