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Titolo:
The MEK1-ERK1/2 signaling pathway promotes compensated cardiac hypertrophyin transgenic mice
Autore:
Bueno, OF; De Windt, LJ; Tymitz, KM; Witt, SA; Kimball, TR; Klevitsky, R; Hewett, TE; Jones, SP; Lefer, DJ; Peng, CF; Kitsis, RN; Molkentin, JD;
Indirizzi:
Univ Cincinnati, Childrens Hosp, Med Ctr, Dept Pediat,Div Mol Cardiovasc Biol, Cincinnati, OH 45229 USA Univ Cincinnati Cincinnati OH USA 45229 sc Biol, Cincinnati, OH 45229 USA LSU, Hlth Sci Ctr, Dept Mol & Cellular Physiol, Shreveport, LA 71130 USA LSU Shreveport LA USA 71130 & Cellular Physiol, Shreveport, LA 71130 USA Albert Einstein Coll Med, Dept Med, Bronx, NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 Dept Med, Bronx, NY 10461 USA Albert Einstein Coll Med, Dept Cell Biol, Bronx, NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 ell Biol, Bronx, NY 10461 USA
Titolo Testata:
EMBO JOURNAL
fascicolo: 23, volume: 19, anno: 2000,
pagine: 6341 - 6350
SICI:
0261-4189(200012)19:23<6341:TMSPPC>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED PROTEIN-KINASE; RAT VENTRICULAR MYOCYTES; GENE-EXPRESSION; CONTRACTILE FAILURE; REGULATED KINASES; CELL HYPERTROPHY; HEART-FAILURE; RECEPTOR; OVEREXPRESSION; PHENYLEPHRINE;
Keywords:
cardiac; cardiomyopathy; hypertrophy; MAPK; transgenic;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
55
Recensione:
Indirizzi per estratti:
Indirizzo: Molkentin, JD Univ Cincinnati, Childrens Hosp, Med Ctr, Dept Pediat,Div Mol Cardiovasc Biol, 3333 Burnet Ave, Cincinnati, OH 45229 USA Univ Cincinnati 3333 Burnet Ave Cincinnati OH USA 45229 USA
Citazione:
O.F. Bueno et al., "The MEK1-ERK1/2 signaling pathway promotes compensated cardiac hypertrophyin transgenic mice", EMBO J, 19(23), 2000, pp. 6341-6350

Abstract

Members of the mitogen-activated protein kinase (MAPK) cascade such as extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) andp38 are implicated as important regulators of cardiomyocyte hypertrophic growth in culture. However, the role that individual MAPK pathways play in vivo has not been extensively evaluated. Here we generated nine transgenic mouse lines with cardiac-restricted expression of an activated MEK1 cDNA in the heart. MEK1 transgenic mice demonstrated concentric hypertrophy withoutsigns of cardiomyopathy or lethality up to 12 months of age. MEK1 transgenic mice showed a dramatic increase in cardiac function, as measured by echocardiography and isolated working heart preparation, without signs of decompensation over time. MEK1 transgenic mice and MEK1 adenovirus-infected neonatal cardiomyocytes each demonstrated ERK1/2, but not p38 or JNK, activation, MEK1 transgenic mice and MEK1 adenovirus-infected cultured cardiomyocytes were also partially resistant to apoptotic stimuli. The results of the present study indicate that the MEK1-ERK1/2 signaling pathway stimulates a physiologic hypertrophy response associated with augmented cardiac function and partial resistance to apoptotsis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 16:12:09