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Titolo:
Protein kinase B/Akt activates c-Jun NH2-terminal kinase by increasing NO production in response to shear stress
Autore:
Go, YM; Boo, YC; Park, H; Maland, MC; Patel, R; Pritchard, KA; Fujio, Y; Walsh, K; Darley-Usmar, V; Jo, H;
Indirizzi:
Georgia Inst Technol, Wallace H Coulter Dept Biomed Engn, Atlanta, GA 30322 USA Georgia Inst Technol Atlanta GA USA 30322 med Engn, Atlanta, GA 30322 USA Emory Univ, Georgia Tech Emory Biomed Engn Dept, Atlanta, GA 30322 USA Emory Univ Atlanta GA USA 30322 y Biomed Engn Dept, Atlanta, GA 30322 USA Univ Alabama, Dept Pathol, Ctr Free Rad Biol, Birmingham, AL 35294 USA Univ Alabama Birmingham AL USA 35294 e Rad Biol, Birmingham, AL 35294 USA Med Coll Wisconsin, Dept Surg, Div Pediat Surg, Milwaukee, WI 53226 USA Med Coll Wisconsin Milwaukee WI USA 53226 t Surg, Milwaukee, WI 53226 USA Tufts Univ, Sch Med, Boston, MA 02135 USA Tufts Univ Boston MA USA 02135Tufts Univ, Sch Med, Boston, MA 02135 USA St Elizabeths Med Ctr, Div Cardiovasc Res, Boston, MA 02135 USA St Elizabeths Med Ctr Boston MA USA 02135 ovasc Res, Boston, MA 02135 USA
Titolo Testata:
JOURNAL OF APPLIED PHYSIOLOGY
fascicolo: 4, volume: 91, anno: 2001,
pagine: 1574 - 1581
SICI:
8750-7587(200110)91:4<1574:PKBACN>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; SIGNAL-REGULATED KINASE; VASCULAR ENDOTHELIAL-CELLS; DEPENDENT ACTIVATION; GROWTH-FACTOR; CA2+-INDEPENDENT ACTIVATION; SUPEROXIDE-DISMUTASE; CAROTID BIFURCATION; GENE-EXPRESSION; KAPPA-B;
Keywords:
endothelial cells; mitogen-activated protein kinase; atherosclerosis; endothelial nitric oxide synthase; mechanosensing;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Jo, H Emory Univ, Georgia Tech Emory Biomed Engn Dept, 303D WMB, Atlanta, GA 30322 USA Emory Univ 303D WMB Atlanta GA USA 30322 WMB, Atlanta, GA 30322 USA
Citazione:
Y.M. Go et al., "Protein kinase B/Akt activates c-Jun NH2-terminal kinase by increasing NO production in response to shear stress", J APP PHYSL, 91(4), 2001, pp. 1574-1581

Abstract

Laminar shear stress activates c-Jun NH2-terminal kinase (JNK) by the mechanisms involving both nitric oxide (NO) and phosphatidylinositide 3-kinase (PI3K). Because protein kinase B (Akt), a downstream effector of PI3K, has been shown to phosphorylate and activate endothelial NO synthase, we hypothesized that Akt regulates shear-dependent activation of JNK by stimulating NO production. Here, we examined the role of Akt in shear-dependent NO production and JNK activation by expressing a dominant negative Akt mutant (Akt(AA)) and a constitutively active mutant (Akt(Myr) in bovine aortic endothelial cells (BAEC). As expected, pretreatment of BAEC with the PI3K inhibitor (wortmannin) prevented shear-dependent stimulation of Akt and NO production. Transient expression of AktAA in BAEC by using a recombinant adenoviralconstruct inhibited the shear-dependent stimulation of NO production and JNK activation. However, transient expression of Akt(Myr) using a recombinant adenoviral construct did not induce JNK activation. This is consistent with our previous finding that NO is required, but not sufficient on its own,to activate JNK in response to shear stress. These results and our previous findings strongly suggest that shear stress triggers activation of PI3K, Akt, and endothelial NO synthase, leading to production of NO, which (alongwith O-2(-), which is also produced by shear) activates Ras-JNK pathway. The regulation of Akt, NO, and JNK by shear stress is likely to play a critical role in its antiatherogenic effects.

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Documento generato il 23/01/21 alle ore 03:46:38