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Titolo:
Fluid shear stress reduces 11 beta-hydroxysteroid dehydrogenase type 2
Autore:
Lanz, CB; Causevic, M; Heiniger, C; Frey, FJ; Frey, BM; Mohaupt, MG;
Indirizzi:
Univ Bern, Div Nephrol Hypertens, Bern, Switzerland Univ Bern Bern Switzerland rn, Div Nephrol Hypertens, Bern, Switzerland
Titolo Testata:
HYPERTENSION
fascicolo: 1, volume: 37, anno: 2001,
pagine: 160 - 169
SICI:
0194-911X(200101)37:1<160:FSSR1B>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
APPARENT MINERALOCORTICOID EXCESS; INTRAUTERINE GROWTH-RETARDATION; CHORIOCARCINOMA JEG-3 CELLS; FOCAL ADHESION KINASE; NECROSIS-FACTOR-ALPHA; UTEROPLACENTAL CIRCULATION; DOPPLER ULTRASOUND; ENDOTHELIAL-CELLS; TYROSINE KINASES; LEUKOTRIENE B-4;
Keywords:
11 beta-hydroxysteroid dehydrogenase; shear stress; cortisol; hypertension; focal adhesion; cytoskeleton;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Mohaupt, MG Univ Hosp Bern, Div Nephrol Hypertens, CH-3010 Bern, Switzerland Univ Hosp Bern Bern Switzerland CH-3010 10 Bern, Switzerland
Citazione:
C.B. Lanz et al., "Fluid shear stress reduces 11 beta-hydroxysteroid dehydrogenase type 2", HYPERTENSIO, 37(1), 2001, pp. 160-169

Abstract

In pregnancy, invading trophoblasts represent the inner vascular border ofmaternal spiral arteries and are exposed to elevated shear stress (ss) in hypertensive disorders. Intracellular cortisol availability is regulated by11 beta -hydroxysteroid dehydrogenases (11 beta -HSDs), thus determining body fluid volume and vascular responses. The impact of ss on 11 beta -HSD2 activity was studied in the human JEG-3 cell line, a model for trophoblasts. JEG-3 cells do not express 11 beta -HSD1; however, 11 beta -HSD2 message and activity are measured via cortisol/cortisone conversion in cell lysates, and both are reduced by ss. The reduction in 11 beta -HSD2 activity via ss is dose dependent and completely reversible after the discontinuation of ss. cAMP-dependent protein kinase A activation increased the 11 beta -HSD2 activity yet did not prevent the ss response. The ss response was completely protein kinase C independent. The mitogen-activated protein kinase kinaseinhibitor PD-098059 enhanced 11 beta -HSD2 activity in static conditions yet only ameliorated the ss effect. Cytochalasin D disrupts focal adhesion (FA)-cytoskeleton interactions and abolished the ss-induced tyrosine phosphorylation of FA kinase dose-dependently, thus maintaining 11 beta -HSD2 activity. The 11 beta -HSD2 activity was only partially restored by the tyrosine kinase inhibitor genistein; however, herbimycin A almost completely abolished the ss effect on 11 beta -HSD2 activity. In conclusion, JEG-3 cells express 11 beta -HSD2, which is downregulated by ss. Regulatory mechanisms involve transcriptional control and require intact FA-cytoskeleton signaling and phosphorylation of FA kinase. Thus, ss adds to an enhanced intracellular availability of cortisol, which may ultimately support a vasoconstrictivevascular response.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/12/18 alle ore 23:22:31