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Titolo:
Upregulation of vasopressin V-1A receptor mRNA and protein in vascular smooth muscle cells following cyclosporin A treatment
Autore:
Cottet-Maire, F; Avdonin, PV; Roulet, E; Buetler, TM; Mermod, N; Ruegg, UT;
Indirizzi:
Univ Lausanne, Sch Pharm, BEP, Pharmacol Grp, CH-1015 Lausanne, Switzerland Univ Lausanne Lausanne Switzerland CH-1015 CH-1015 Lausanne, Switzerland Russian Acad Sci, Inst Dev Biol, Moscow, Russia Russian Acad Sci Moscow Russia Acad Sci, Inst Dev Biol, Moscow, Russia Univ Lausanne, EPFL, UNIL, Ctr Biotechnol,Lab Mol Biotechnol, CH-1015 Lausanne, Switzerland Univ Lausanne Lausanne Switzerland CH-1015 CH-1015 Lausanne, Switzerland Univ Lausanne, Inst Biol Anim, CH-1015 Lausanne, Switzerland Univ Lausanne Lausanne Switzerland CH-1015 CH-1015 Lausanne, Switzerland
Titolo Testata:
BRITISH JOURNAL OF PHARMACOLOGY
fascicolo: 4, volume: 132, anno: 2001,
pagine: 909 - 917
SICI:
0007-1188(200102)132:4<909:UOVVRM>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
MESSENGER-RNA STABILITY; ANGIOTENSIN-II RECEPTORS; A-INDUCED HYPERTENSION; ARGININE-VASOPRESSIN; RENAL VASOCONSTRICTION; SIGNAL TRANSDUCTION; MOLECULAR-CLONING; CALCIUM EFFLUX; RAT V1A; EXPRESSION;
Keywords:
cyclosporin A; hypertension; smooth muscle cells; vasopressin V-1 receptor; promoter; quantitative polymerase chain reaction; reporter gene assay; receptor internalization; receptor upregulation; mRNA stability;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Ruegg, UT Univ Lausanne, Sch Pharm, BEP, Pharmacol Grp, CH-1015 Lausanne, Switzerland Univ Lausanne Lausanne Switzerland CH-1015 usanne, Switzerland
Citazione:
F. Cottet-Maire et al., "Upregulation of vasopressin V-1A receptor mRNA and protein in vascular smooth muscle cells following cyclosporin A treatment", BR J PHARM, 132(4), 2001, pp. 909-917

Abstract

1 The major side effects of the immunosuppressive drug cyclosporin A (CsA)are hypertension and nephrotoxicity. It is likely that both are caused by local vasoconstriction. 2 We have shown previously that 20 h treatment of rat vascular smooth muscle cells (VSMC) with therapeutically relevant CsA concentrations increased the cellular response to [Arg*]vasopressin (AVP) by increasing about2 fold the number of vasopressin receptors.3 Displacement experiments using a specific antagonist of the vasopressin V-1A receptor (V1AR) showed that the vasopressin binding sites present in VSMC were exclusively receptors of the VIA subtype.4 Receptor internalization studies revealed that CsA (10(-6) M)did not significantly alter AVP receptor trafficking.5 V1AR mRNA was increased by CsA, as measured by quantitative polymerase chain reaction. Time-course studies indicated that the increase in mRNA preceded cell surface expression of the receptor. as measured by hormone binding.6 A direct effect of CsA on the V1AR promoter was investigated using VSMC transfected with a V1AR promoter-luciferase reporter construct. Surprisingly, CsA did not increase. but rather slightly reduced V1AR promoter activity. This effect was independent of the cyclophilin-calcineurin pathway.7 Measurement of V1AR mRNA decay in the presence of the transcription inhibitor actinomycin D revealed that CsA increased the half-life of V1AR mRNA about 2 fold.8 In conclusion, CsA increased the response of VSMC to AVP by upregulatingV1AR expression through stabilization of its mRNA. This could be a key mechanism in enhanced Vascular responsiveness induced by CsA, causing both hypertension and. via renal vasoconstriction, reduced glomerular filtration.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 23:37:49