Heterogeneity of oxidant stress in the reoxygenated developing heart

Raddatz, Eric; Rochat, Anne-Catherine

doi:10.1016/s0022-2828(02)90932-6

Cited by 3 publications

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Regarding the response to oxygen deprivation and reoxygenation, some differential sensitivity is expected within the embryonic heart since anoxic tolerance [9], energy metabolism [21], Ca 2? handling [22,23], myofilaments [24], oxidative stress [25], sensitivity to NO [26], and electrical [27] and contractile [10] properties vary from one cardiac region to another. These important developmental, structural, and functional differences combined with the fact that activation of MAPKs depends on the nature of the stimuli and the celltype [28] lead us to hypothesize that ERK, p38, and JNK pathways display distinct spatio-temporal patterns of activation in response to a transient anoxic stress.…”

Section: Introductionmentioning

confidence: 99%

Transient anoxia and oxyradicals induce a region-specific activation of MAPKs in the embryonic heart

et al. 2010

Self Cite

View full text Add to dashboard Cite

We have previously reported in the early septating embryonic heart that electromechanical disturbances induced by anoxia-reoxygenation are distinct in atria, ventricle, and outflow tract, and are attenuated in ventricle by opening of mitochondrial K(ATP) (mitoK(ATP)) channels. Here, we assessed the regional activation of mitogen-activated protein kinases (MAPKs) ERK, p38, and JNK in response to anoxia-reoxygenation and H(2)O(2). Hearts isolated from 4-day-old chick embryos were subjected to 30-min anoxia and 60-min reoxygenation or exposed to H(2)O(2) (50 microM-1 mM). The temporal pattern of activation of ERK, p38, and JNK in atria, ventricle, and outflow tract was determined using immunoblotting and/or kinase assay. The effect of the mitoK(ATP) channel opener diazoxide (50 microM) on JNK phosphorylation was also analyzed. Under basal conditions, total ERK and JNK were homogeneously distributed within the heart, whereas total p38 was the lowest in outflow tract. The phosphorylated/total form ratio of each MAPK was similar in all regions. Phosphorylation of ERK increased in atria and ventricle at the end of reoxygenation without change in outflow tract. Phosphorylation of p38 was augmented by anoxia in the three regions, and returned to basal level at the end of reoxygenation except in the outflow tract. JNK activity was not altered by anoxia-reoxygenation in atria and outflow tract. In ventricle, however, the diazoxide-inhibitable peak of JNK activity known to occur during reoxygenation was not accompanied by a change in phosphorylation level. H(2)O(2) over 500 microM impaired cardiac function, phosphorylated ERK in all the regions and p38 in atria and outflow tract, but did not affect JNK phosphorylation. At a critical stage of early cardiogenesis, anoxia, reoxygenation, exogenous H(2)O(2) and opening of mitoK(ATP) channels can subtly modulate ERK, p38, and JNK pathways in a region-specific manner.

show abstract

Section: Introductionmentioning

confidence: 99%

Transient anoxia and oxyradicals induce a region-specific activation of MAPKs in the embryonic heart

et al. 2010

Self Cite

View full text Add to dashboard Cite

show abstract

“…We previously characterized the chrono-, dromo-, and inotropic responses of the isolated embryonic chick heart (4 -5 days old) to anoxia-reoxygenation (30,34). We also found that this preparation is subjected to an oxidative stress during reoxygenation (28) similar to reperfused cardiac cells obtained from 10-day-old chick embryo (41,45). Interestingly, the postischemic protection of embryonic ventricular myocytes afforded by mitoK ATP channel opening involves ROS and/or NO production (6,19).…”

mentioning

confidence: 99%

mitoK_ATP channel activation in the postanoxic developing heart protects E-C coupling via NO-, ROS-, and PKC-dependent pathways

Sarre¹,

Lange²,

Kučera³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

View full text Add to dashboard Cite

Whereas previous studies have shown that opening of the mitochondrial ATP-sensitive K(+) (mitoK(ATP)) channel protects the adult heart against ischemia-reperfusion injury, it remains to be established whether this mechanism also operates in the developing heart. Isolated spontaneously beating hearts from 4-day-old chick embryos were subjected to 30 min of anoxia followed by 60 min of reoxygenation. The chrono-, dromo-, and inotropic disturbances, as well as alterations of the electromechanical delay (EMD), reflecting excitation-contraction (E-C) coupling, were investigated. Production of reactive oxygen species (ROS) in the ventricle was determined using the intracellular fluorescent probe 2',7'-dichlorofluorescin (DCFH). Effects of the specific mitoK(ATP) channel opener diazoxide (Diazo, 50 microM) or the blocker 5-hydroxydecanoate (5-HD, 500 microM), the nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 50 microM), the antioxidant N-(2-mercaptopropionyl)glycine (MPG, 1 mM), and the PKC inhibitor chelerythrine (Chel, 5 microM) on oxidative stress and postanoxic functional recovery were determined. Under normoxia, the baseline parameters were not altered by any of these pharmacological agents, alone or in combination. During the first 20 min of postanoxic reoxygenation, Diazo doubled the peak of ROS production and, interestingly, accelerated recovery of ventricular EMD and the PR interval. Diazo-induced ROS production was suppressed by 5-HD, MPG, or L-NAME, but not by Chel. Protection of ventricular EMD by Diazo was abolished by 5-HD, MPG, L-NAME, or Chel, whereas protection of the PR interval was abolished by L-NAME exclusively. Thus pharmacological opening of the mitoK(ATP) channel selectively improves postanoxic recovery of cell-to-cell communication and ventricular E-C coupling. Although the NO-, ROS-, and PKC-dependent pathways also seem to be involved in this cardioprotection, their interrelation in the developing heart can differ markedly from that in the adult myocardium.

show abstract

Physiopathology of the embryonic heart (with special emphasis on hypoxia and reoxygenation)

Raddatz

Gardier

Sarre

2006

Annales de Cardiologie et d'Angéiologie

View full text Add to dashboard Cite

Heterogeneity of oxidant stress in the reoxygenated developing heart

Cited by 3 publications

References 0 publications

Transient anoxia and oxyradicals induce a region-specific activation of MAPKs in the embryonic heart

Transient anoxia and oxyradicals induce a region-specific activation of MAPKs in the embryonic heart

mitoK_ATP channel activation in the postanoxic developing heart protects E-C coupling via NO-, ROS-, and PKC-dependent pathways

Physiopathology of the embryonic heart (with special emphasis on hypoxia and reoxygenation)

Contact Info

Product

Resources

About

Heterogeneity of oxidant stress in the reoxygenated developing heart

Cited by 3 publications

References 0 publications

Transient anoxia and oxyradicals induce a region-specific activation of MAPKs in the embryonic heart

Transient anoxia and oxyradicals induce a region-specific activation of MAPKs in the embryonic heart

mitoKATP channel activation in the postanoxic developing heart protects E-C coupling via NO-, ROS-, and PKC-dependent pathways

Physiopathology of the embryonic heart (with special emphasis on hypoxia and reoxygenation)

Contact Info

Product

Resources

About

mitoK_ATP channel activation in the postanoxic developing heart protects E-C coupling via NO-, ROS-, and PKC-dependent pathways