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Titolo:
Regulation of the nitric oxide synthase-nitric oxide-cGMP pathway in rat mesenteric endothelial cells
Autore:
Papapetropoulos, A; Andreopoulos, S; Go, CY; Hoque, A; Fuchs, LC; Catravas, JD;
Indirizzi:
Med Coll Georgia, Vasc Biol Ctr, Augusta, GA 30912 USA Med Coll Georgia Augusta GA USA 30912 asc Biol Ctr, Augusta, GA 30912 USA Med Coll Georgia, Dept Pharmacol & Toxicol, Augusta, GA 30912 USA Med CollGeorgia Augusta GA USA 30912 ol & Toxicol, Augusta, GA 30912 USA Univ Athens, Evagelismos Hosp, Dept Crit Care & Pulm Serv, George P Livanos Lab, Athens 10675, Greece Univ Athens Athens Greece 10675 orge P Livanos Lab, Athens 10675, Greece
Titolo Testata:
JOURNAL OF APPLIED PHYSIOLOGY
fascicolo: 6, volume: 91, anno: 2001,
pagine: 2553 - 2560
SICI:
8750-7587(200112)91:6<2553:ROTNOS>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
TYROSINE KINASE INHIBITORS; SMOOTH-MUSCLE CELLS; DEPENDENT RELAXATION; MESSENGER-RNA; VASCULAR BED; IN-VIVO; EXPRESSION; HETEROGENEITY; ACETYLCHOLINE; CYTOSKELETON;
Keywords:
endothelium; guanylyl cyclase; guanosine 3 ',5 '-cyclic monophosphate; microtubules;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Catravas, JD Med Coll Georgia, Vasc Biol Ctr, Augusta, GA 30912 USA Med Coll Georgia Augusta GA USA 30912 Augusta, GA 30912 USA
Citazione:
A. Papapetropoulos et al., "Regulation of the nitric oxide synthase-nitric oxide-cGMP pathway in rat mesenteric endothelial cells", J APP PHYSL, 91(6), 2001, pp. 2553-2560

Abstract

Most of the available data on the nitric oxide (NO) pathway in the vasculature is derived from studies performed with cells isolated from conduit arteries. We investigated the expression and regulation of components of the NO synthase (NOS)-NO-cGMP pathway in endothelial cells from the mesenteric vascular bed. Basally, or in response to bradykinin, cultured mesenteric endothelial cells (MEC) do not release NO and do not express endothelial NOS protein. MEC treated with cytokines, but not untreated cells, express inducible NOS (iNOS) mRNA and protein, increase nitrite release, and stimulate cGMP accumulation in reporter smooth muscle cells. Pretreatment of MEC with genistein abolished the cytokine-induced iNOS expression. On the other hand,exposure of MEC to the microtubule depolymerizing agent colchicine did notaffect the cytokine-induced increase in nitrite formation and iNOS proteinexpression, whereas it inhibited the induction of iNOS in smooth muscle cells. Collectively, our findings demonstrate that MEC do not express endothelial NOS but respond to inflammatory stimuli by expressing iNOS, a process that is blocked by tyrosine kinase inhibition but not by microtubule depolymerization.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/06/20 alle ore 23:53:07