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Titolo:
Effects of norepinephrine on apoptosis in rat neonatal cardiomyocytes
Autore:
Shyu, KG; Kuan, PL; Chang, ML; Wang, BW; Huang, FY;
Indirizzi:
Shin Kong Wu Ho Su Mem Hosp, Dept Internal Med, Div Cardiol, Taipei, Taiwan Shin Kong Wu Ho Su Mem Hosp Taipei Taiwan , Div Cardiol, Taipei, Taiwan Shin Kong Wu Ho Su Mem Hosp, Dept Anesthesia, Taipei, Taiwan Shin Kong Wu Ho Su Mem Hosp Taipei Taiwan pt Anesthesia, Taipei, Taiwan
Titolo Testata:
JOURNAL OF THE FORMOSAN MEDICAL ASSOCIATION
fascicolo: 5, volume: 99, anno: 2000,
pagine: 412 - 418
SICI:
0929-6646(200005)99:5<412:EONOAI>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
MYOCYTE CELL-DEATH; HEART-FAILURE; CARDIAC MYOCYTES; ANGIOTENSIN-II; IN-VITRO; VENTRICULAR MYOCYTES; PRESSURE-OVERLOAD; C-FOS; GENE; EXPRESSION;
Keywords:
apoptosis; myocytes; norepinephrine; adrenergic antagonist; Mcl-1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Shyu, KG Shin Kong Wu Ho Su Mem Hosp, Dept Internal Med, Div Cardiol, 95 Wen Chang Rd, Taipei, Taiwan Shin Kong Wu Ho Su Mem Hosp 95 Wen Chang Rd Taipei Taiwan aiwan
Citazione:
K.G. Shyu et al., "Effects of norepinephrine on apoptosis in rat neonatal cardiomyocytes", J FORMOS ME, 99(5), 2000, pp. 412-418

Abstract

Background and purpose: Norepinephrine (NE) is elevated in heart failure and can induce apoptosis in adult cardiac myocytes. However, it is not knownwhether NE can induce apoptosis in neonatal cardiac myocytes. This study examined the ability of NE to stimulate apoptosis in rat neonatal cardiac myocytes in vitro. Methods: Neonatal rat cardiac myocytes were exposed to NE alone, NE + propranolol, or NE + prazosin for 24 hours. Apoptosis was assayed by DNA laddering with agarose gel electrophoresis and immunofluorescent terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. Reverse transcription polymerase chain reaction was used to evaluate the expression of Mcl-1. Creatine kinase activity in the cultured medium was used asa measure of the toxicity of NE an myocytes. Results: NE increased DNA laddering on agarose gel electrophoresis and increased the number of apoptotic cells in a dose-dependent manner. No increase in apoptosis was found in response to SE doses between 1 and 50 mu mol/L. NE at concentrations of 100 to 400 mu mol/L increased apoptosis from 10% to 31% of cells. The ability of NE to stimulate apoptosis in rat neonatal cardiac myocytes was completely blocked by propranolol, but not prazosin. NE treatment at high concentrations sharply reduced the level of Mcl-1 mRNA, coincident with the increase in the number of apoptotic cells. Creatine kinase activity in the cultured medium was similar among the controls and NE-treated myocytes. Conclusions: Our results showed that NE at high concentrations stimulated apoptosis in rat neonatal cardiac myocytes in vitro. Apoptosis induced by NE was associated with do down-regulation of Mcl-1. However, NE at the same concentration was not toxic to rat neonatal cardiac myocytes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/12/20 alle ore 15:21:07