Carvedilol effectively blocks oxidative stress-mediated downregulation of sarcoplasmic reticulum Ca2+-ATPase 2 gene transcription through modification of Sp1 binding

Koitabashi, Norimichi; Arai, M.; Tomaru, Koichi; Takizawa, Takeo; Watanabe, Atai; Niwano, Kazuo; Yokoyama, Tetsuji; Wuytack, Frank; Periasamy, Muthu; Nagai, Ryozo; Kurabayashi, Masahiko

doi:10.1016/j.bbrc.2004.12.139

Cited by 52 publications

(33 citation statements)

References 29 publications

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“…For instance, oxidative stress lowered binding of Sp1 and Sp3 to the proximal region of SERCA2 promoter, leading to down-regulation of the gene, while an antioxidant carvedilol could, on the other hand, restore the binding of these transcription factors (Koitabashi et al, 2005). Similar observations were found in another oxidative stress-regulated gene, vascular endothelial growth factor-A (VEGF-A) (Schäfer et al, 2003).…”

Section: Discussionmentioning

confidence: 58%

Regulation of RASSF1A in nasopharyngeal cells and its response to UV irradiation

Lee

Chow

et al. 2009

Gene

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Section: Discussionmentioning

confidence: 58%

Regulation of RASSF1A in nasopharyngeal cells and its response to UV irradiation

Lee

Chow

et al. 2009

Gene

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“…In this context, there seems to be no specific differences in the Ca 2+ handling effects of CAN or other angiotensin-II antagonists like valsartan. Binding of angiotensin II to the postsynaptic AT1 receptor may also decrease SR Ca 2+ uptake activity by decreasing the level of expression of SERCA2a mRNA 28 and also by increasing PKCactivity, which in turn directly phosphorylates serine 67 in inhibitor 1, thereby augmenting the activity of protein phosphatase-1 (PP1) and causing the hypophosphorylation of PLN. 29 Takeishi et al 30 also demonstrated that angiotensin-II inhibition by ramipril attenuates PKC translocation and prevents downregulation of SERCA2a and PLB protein expressions in pressure-overload hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

AT1 Receptor Antagonist Restores Cardiac Ryanodine Receptor Function, Rendering Isoproterenol-Induced Failing Heart Less Susceptible to Ca2+-Leak Induced by Oxidative Stress

Tokuhisa

Yano

Obayashi

et al. 2006

Circ J

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uring the development of heart failure, abnormal regulation of intracellular Ca 2+ has been shown to contribute to the impaired cardiac contraction and relaxation. 1,2 Several lines of evidence have accumulated demonstrating that decreased activity or expression of Ca 2+ -ATPase (SERCA2a) in the sarcoplasmic reticulum (SR) may be an important cause of heart failure. 3,4 In addition, abnormal Ca 2+ -leakage through the SR Ca 2+ release channel, known as the ryanodine receptor (RyR2), has been demonstrated as a possible trigger for the development of heart failure. 5,6 In those studies of cases of heart failure, Ca 2+ -leak was found to be induced by the dissociation of FKBP12.6 from the RyR2 as a result of the hyperphosphorylation of the RyR2. Restoration of the defective FKBP12.6-mediated stabilization of the RyR2 either by a -blocker 7 or by a new cardioprotective agent, JTV519, 8 improved cardiac function during the development of heart failure.Angiotensin II antagonism not only prevents hypertrophy and/or interstitial fibrosis, 9,10 but also attenuates the downregulation of SERCA2a and improves intracellular Ca 2+ handling. 11,12 In a canine model of heart failure, we recently demonstrated that during the development of pacinginduced heart failure, valsartan preserved the density ofreceptors and concurrently restored SR function (increase in Ca 2+ -uptake and prevention of Ca 2+ -leak). 13 By acting on the presynaptic angiotensin-II receptor, valsartan may inhibit norepinephrine release and stimulate norepinephrine uptake back into the synaptic pool, in turn leading to a reduction in the adrenergic signal being transmitted into the cell. The fewer adrenergic signals may lead to a decrease in the level of RyR2-phosphorylation, and an inhibition of Ca 2+ -leak through the receptor. 13 Although valsartan did not improve resting cardiac function, it did enhance the contractility reserve, as suggested by an enhanced dobutamine response. 13 Chronic norepinephrine release from the synaptic pool in the hyperadrenergic state plays a crucial role in the pathogenesis of heart failure, regardless of the initial cause of the myocardial damage (hypertension, myocardial ischemia, cardiomyopathy etc). 14,15 However, heart failure is a complex disorder, and many other factors (oxidative stress, apoptosis etc) have been shown to concurrently influence the development of contractile dysfunction and/or the left ventricular (LV) remodeling process, together with the de- Background The Ca 2+ regulatory proteins in the sarcoplasmic reticulum (SR) play a key role in the pathogenesis of heart failure. In the present study the effect of chronic -receptor-stimulation on cardiac and SR functions was assessed, with or without angiotensin-II receptor antagonist treatment recently reported to have anti--adrenergic activity. Methods and ResultsRats were treated with isoproterenol with (+) or without (-) candesartan (CAN) and then SR vesicles were isolated from the left ventricular muscle. Both Ca 2+ -uptake and the amount of SR Ca 2+ -ATPas...

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“…c-kit + cardiac progenitor cells are also known to express higher levels of SOD, and, therefore, coupled with their capacity to increase the expression of SOD in response to oxidative stress, are resistant to ROS-induced cell death (136). Khan et al reported that ckit + cardiac progenitor cells switch the expression of the subtype of adrenergic receptor (AR) from b2-AR to b1-AR once they are committed to myocyte differentiation, and treatment of b-blockers, which are known to have antioxidant properties (76), can enhance their survival and proliferation (69). This might suggest that c-kit + cells are especially sensitive to oxidative stress when they start differentiation.…”

Section: Antioxidant Response In Cardiac Turnovermentioning

confidence: 99%

Redox Signaling in Cardiac Renewal

Kimura

Muralidhar

Canseco

et al. 2014

Antioxidants & Redox Signaling

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Significance: Utilizing oxygen (O 2 ) through mitochondrial oxidative phosphorylation enables organisms to generate adenosine triphosphate (ATP) with a higher efficiency than glycolysis, but it results in increased reactive oxygen species production from mitochondria, which can result in stem cell dysfunction and senescence. Recent Advances: In the postnatal organism, the hematopoietic system represents a classic example of the role of stem cells in cellular turnover and regeneration. However, in other organs such as the heart, both the degree and source of cellular turnover have been heavily contested. Critical Issues: Although recent evidence suggests that the major source of the limited cardiomyocyte turnover in the adult heart is cardiomyocyte proliferation, the identity and potential role of undifferentiated cardiac progenitor cells remain controversial. Several types of cardiac progenitor cells have been identified, and several studies have identified an important role of redox and metabolic regulation in survival and differentiation of cardiac progenitor cells. Perhaps a simple way to approach these controversies is to focus on the multipotentiality characteristics of a certain progenitor population, and not necessarily its ability to give rise to all cell types within the heart. In addition, it is important to note that cycling cells in the heart may express markers of differentiation or may be truly undifferentiated, and for the purpose of this review, we will refer to these cycling cells as progenitors. Future Directions: We propose that hypoxia, redox signaling, and metabolic phenotypes are major regulators of cardiac renewal, and may prove to be important therapeutic targets for heart regeneration. Antioxid. Redox Signal. 21, 1660-1673.

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Carvedilol effectively blocks oxidative stress-mediated downregulation of sarcoplasmic reticulum Ca2+-ATPase 2 gene transcription through modification of Sp1 binding

Cited by 52 publications

References 29 publications

Regulation of RASSF1A in nasopharyngeal cells and its response to UV irradiation

Regulation of RASSF1A in nasopharyngeal cells and its response to UV irradiation

AT1 Receptor Antagonist Restores Cardiac Ryanodine Receptor Function, Rendering Isoproterenol-Induced Failing Heart Less Susceptible to Ca2+-Leak Induced by Oxidative Stress

Redox Signaling in Cardiac Renewal

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