Involvement of tyrosine kinase in peroxynitrite-induced preconditioning in rat isolated heart

Söylemez, Sibel; Demiryürek, Abdullah Tuncay; Kanzik, I

doi:10.1016/s0014-2999(03)01377-3

Cited by 7 publications

(8 citation statements)

References 34 publications

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“…Previous work performed in other laboratories using skin fibroblasts has reported that PN can cooperate or interfere with tyrosine kinase receptor‐mediated signaling pathways (Klotz et al. 2002; Söylemez et al. 2003).…”

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confidence: 99%

Inhibition of PTEN by peroxynitrite activates the phosphoinositide‐3‐kinase/Akt neuroprotective signaling pathway

Delgado‐Esteban

Martı́n-Zanca

Martin

et al. 2007

Journal of Neurochemistry

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Peroxynitrite is usually considered as a neurotoxic nitric oxidederivative. However, an increasing body of evidence suggests that, at low concentrations, peroxynitrite affords transient cytoprotection, both in vitro and in vivo. Here, we addressed the signaling mechanism responsible for this effect, and found that rat cortical neurons in primary culture acutely exposed to peroxynitrite (0.1 mmol/L) rapidly elicited Akt-Ser 473 phos- Peroxynitrite (PN), the product of the reaction between nitric oxide (NO) and superoxide (O 2•) ) (Blough and Zafiriou 1985), is spontaneously formed in mammalian cells under physiological conditions (Radi et al. 2001;Possel et al. 2002). Initial work addressing the pathophysiology of PN yielded the widely accepted notion that this compound would be the long-term cytotoxic NO-derivative (Beckman et al. 1990;Radi et al. 1991). Peroxynitrite involvement in cytotoxicity is documented by detecting protein 3-nitrotyrosination, i.e. the 'footprinting' like evidence for in situ PN formation (Ischiropoulos et al. 1992;Greenacre and Ischiropoulos 2001;Beal 2002), associated with neurodegeneration and other disorders (Bolaños et al. 1997;Lipton 1999;Guix et al. 2005). However, in apparent contradiction with Received November 8, 2006; revised manuscript received January 5, 2007; accepted January 9, 2007. Address correspondence and reprint requests to Prof. Juan P. Bolaños, Departamento de Bioquímica y Biología Molecular, Campus Miguel de Unamuno, Universidad de Salamanca, 37007 Salamanca, Spain. E-mail: jbolanos@usal.esAbbreviations used: 7-AAD, 7-amino-actinomycin D; Akt, protein kinase B; APC, allophycocyanin; BDNF, brain-derived neurotrophic factor; CAT, catalase; DAPI, 4¢-6-diamidino-2-phenylindole; GSH, glutathione ethyl ester; GFP, green fluorescent protein; Luc, luciferase; RNAi, RNA interference; PI3K, phosphoinositide-3-kinase; PFK-1, 6-phosphofructo-1-kinase; PN, peroxynitrite; PTP, protein tyrosine phosphatase; PTEN, phosphatase with tensin homology; shRNA, small hairpin RNA; SIN-1, 3-morpholinosydnonimine; SOD, superoxide dismutase; Trk, neurotrophin tyrosine kinase receptor.

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confidence: 99%

Inhibition of PTEN by peroxynitrite activates the phosphoinositide‐3‐kinase/Akt neuroprotective signaling pathway

Delgado‐Esteban

Martı́n-Zanca

Martin

et al. 2007

Journal of Neurochemistry

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“…Both Ca 2þ -depletion and repletion, as well as tachycardia induced preconditioning, have also been shown to exert protective effects against I/R injury but their mechanisms are different from each other [237][238][239]. Different trigger mechanisms including the low concentrations of oxyradicals, as well as different oxidants such as NO, peroxynitrite and H 2 O 2 , have been shown to be involved in the ischemic preconditioning [218,237,[240][241][242][243][244][245][246][247][248][249][250][251][252][253][254][255][256]. Both tyrosine kinase and mitogen-activated protein kinase, in addition to different isoforms of protein kinase C, have also been demonstrated to participate in ischemic preconditioning [257][258][259][260][261][262][263][264][265][266][267][268].…”

Section: Subcellular Modification Due To Ischemic Preconditioningmentioning

confidence: 99%

Potential role and mechanisms of subcellular remodeling in cardiac dysfunction due to ischemic heart disease

Dhalla

Saini

Tappia

et al. 2007

Journal of Cardiovascular Medicine

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Several studies have revealed varying degrees of changes in sarcoplasmic reticular and myofibrillar activities, protein content, gene expression and intracellular Ca-handling during cardiac dysfunction due to ischemia-reperfusion (I/R); however, relatively little is known about the sarcolemmal and mitochondrial alterations, as well as their mechanisms in the I/R hearts. Because I/R is associated with oxidative stress and intracellular Ca-overload, it has been indicated that changes in subcellular activities, protein content and gene expression due to I/R are related to both oxidative stress and Ca-overload. Intracellular Ca-overload appears to induce changes in subcellular activities, protein contents and gene expression (subcellular remodeling) by activation of proteases and phospholipases, as well as by affecting the genetic apparatus, whereas oxidative stress is considered to cause oxidation of functional groups of different subcellular proteins in addition to modifying the genetic machinery. Ischemic preconditioning, which is known to depress the development of both intracellular Ca-overload and oxidative stress due to I/R, was observed to attenuate the I/R-induced subcellular remodeling and improve cardiac performance. It is suggested that a combination therapy with antioxidants and interventions, which reduce the development of intracellular Ca-overload, may improve cardiac function by preventing or attenuating the occurrence of subcellular remodeling due to ischemic heart disease. It is proposed that defects in the activities of subcellular organelles may serve as underlying mechanisms for I/R-induced cardiac dysfunction under acute conditions, whereas subcellular remodeling due to alterations in gene expression may explain the impaired cardiac performance under chronic conditions of I/R.

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“…1 Otherwise, it was also shown that genistein abolishes the antiarrhythmic effect of ischemic preconditioning in Langendorf perfused rats. 9 Söylemez et al 10 observed that genistein alone was not found to be effective on the ischemia-induced arrhythmia. Long-term administration of genistein and its effects on the ischemia or reperfusion induced arrhythmia were not studied previously.…”

Section: Introductionmentioning

confidence: 99%

The effect of acute or long-term genistein administration on the ischemia/reperfusion-induced arrhythmia in rats

Bozdoğan

Ekşioğlu

Erim

et al. 2018

MOJAP

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The cardiovascular disease and sudden death due to the occlusion of coronary artery increases in women after menopause. In this study, it was aimed to research the effect of genistein that has been used to decrease the symptom of menopause in women, on the ischemia reperfusion induced arrhythmias. 64 Female and 12 male, 6-7months old Sprague Dowley rats were used in this study. Genistein was applied daily for four weeks in 100ug/kg dose intraperitoneally in one group and acutely in other group, before reperfusion in 1mg/kg dose intravenously. Six minutes myocardial ischemia were produced by the ligation of ramus interventricularis branch of left coronary artery (LAD) and six minutes of reperfusion by releasing of this artery. The type and duration of arrhythmias and the blood pressure recorded in every group during ischemia and reperfusion were analyzed and compared by using one-way ANOVA test and the incidence of arrhythmia and the survival rate by Ki square test. Genistein had no effect on the ischemia and reperfusion induced arrhythmias in male and ovariectomized female rats.

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Involvement of tyrosine kinase in peroxynitrite-induced preconditioning in rat isolated heart

Cited by 7 publications

References 34 publications

Inhibition of PTEN by peroxynitrite activates the phosphoinositide‐3‐kinase/Akt neuroprotective signaling pathway

Inhibition of PTEN by peroxynitrite activates the phosphoinositide‐3‐kinase/Akt neuroprotective signaling pathway

Potential role and mechanisms of subcellular remodeling in cardiac dysfunction due to ischemic heart disease

The effect of acute or long-term genistein administration on the ischemia/reperfusion-induced arrhythmia in rats

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