Oxidative stress stimulates both growth and apoptosis in cardiac myocytes in vitro. We investigated the role of oxidative stress in the initial phases of cardiac remodeling induced in an animal model by volume overload. As plausible candidates for a connection between oxidative stress and cardiomyocyte apoptosis or hypertrophy, we explored the behaviour of two MAPKs, specifically JNK and ERK. At 48 h of overload, the greatest increase in oxidative stress coincided with a peak of cardiomyocyte apoptosis. This was possibly induced through the mitochondrial metabolism, as evidenced by the release of cytochrome c and a significant increase in the active forms of caspase-9 and -3, but not caspase-8. Oxidative stress markers significantly decreased at 96 h of overload, combined with a marked attenuation of apoptosis and the appearance of hypertrophy. The highest levels of JNK and the lowest levels of ERK phosphorylation were observed at 48 h of overload. Conversely, a sharp increase in ERK phosphorylation was detected at 96 h of overload coinciding with the hypertrophic response. Together these results show that oxidative stress is an early and transient event in myocardial volume overload. They suggest that oxidative stress mediates amplitude dependent apoptotic and hypertrophic responses in cardiomyocytes through the selective activation of, respectively, JNK and ERK.

Cardiac volume overload rapidly induces oxidative stress-mediated myocyte apoptosis and hypertrophy / C. FIORILLO; C. NEDIANI; V. PONZIANI; L. GIANNINI; A. CELLI; N. NASSI; L. FORMIGLI; A.M. PERNA; P. NASSI. - In: BIOCHIMICA ET BIOPHYSICA ACTA. MOLECULAR BASIS OF DISEASE. - ISSN 0925-4439. - STAMPA. - 1741:(2005), pp. 173-182. [10.1016/j.bbadis.2005.03.015]

Cardiac volume overload rapidly induces oxidative stress-mediated myocyte apoptosis and hypertrophy

FIORILLO, CLAUDIA;NEDIANI, CHIARA;PONZIANI, VANESSA;GIANNINI, LARA;CELLI, ALESSANDRA;NASSI, NICCOLO';FORMIGLI, LUCIA;NASSI, PAOLO ANTONIO
2005

Abstract

Oxidative stress stimulates both growth and apoptosis in cardiac myocytes in vitro. We investigated the role of oxidative stress in the initial phases of cardiac remodeling induced in an animal model by volume overload. As plausible candidates for a connection between oxidative stress and cardiomyocyte apoptosis or hypertrophy, we explored the behaviour of two MAPKs, specifically JNK and ERK. At 48 h of overload, the greatest increase in oxidative stress coincided with a peak of cardiomyocyte apoptosis. This was possibly induced through the mitochondrial metabolism, as evidenced by the release of cytochrome c and a significant increase in the active forms of caspase-9 and -3, but not caspase-8. Oxidative stress markers significantly decreased at 96 h of overload, combined with a marked attenuation of apoptosis and the appearance of hypertrophy. The highest levels of JNK and the lowest levels of ERK phosphorylation were observed at 48 h of overload. Conversely, a sharp increase in ERK phosphorylation was detected at 96 h of overload coinciding with the hypertrophic response. Together these results show that oxidative stress is an early and transient event in myocardial volume overload. They suggest that oxidative stress mediates amplitude dependent apoptotic and hypertrophic responses in cardiomyocytes through the selective activation of, respectively, JNK and ERK.
2005
1741
173
182
Goal 3: Good health and well-being for people
C. FIORILLO; C. NEDIANI; V. PONZIANI; L. GIANNINI; A. CELLI; N. NASSI; L. FORMIGLI; A.M. PERNA; P. NASSI
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Utilizza questo identificatore per citare o creare un link a questa risorsa: https://hdl.handle.net/2158/26633
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