Curcumin: a potential therapeutic polyphenol, prevents noradrenaline-induced hypertrophy in rat cardiac myocytes

Ahuja, Suchit; Kohli, Shruti; Krishnan, S.; Deepika, Dogra; Sharma, Dinesh Kumar; Rani, Vibha

doi:10.1111/j.2042-7158.2011.01363.x

Cited by 28 publications

(16 citation statements)

References 26 publications

(29 reference statements)

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“…Besides this, cells were separately treated with curcumin alone without NE. Increase in size of terminally differentiated cardiomyocytes, protein content and induction of fetal genes such as ANF are indicators of hypertrophic stress [19]. A reduction in the size of cardiomyocytes was observed after treatment with curcumin under hypertrophic conditions as reported earlier by our group (Figure S2).…”

Section: Resultssupporting

confidence: 80%

“…Embryonic Rat Heart-derived H9c2 cells (NCCS, Pune, India) were cultured and hypertrophic stress was induced using 2 µM NE as previously described [19]. A concentration of 8 µM curcumin as reported earlier by our group was added simultaneous to the NE induction [19].…”

Section: Methodsmentioning

confidence: 99%

“…A concentration of 8 µM curcumin as reported earlier by our group was added simultaneous to the NE induction [19]. Cell size was studied and then analyzed by NIH ImageJ.…”

Section: Methodsmentioning

confidence: 99%

“…Recently, it has been established that curcumin attenuates maladaptive cardiac repair and improves cardiac function by reducing degradation of ECM [18]. Our earlier studies have evaluated its cardioprotective potential by targeting the transcriptional pathway regulating the re-expression of fetal cardiac gene program [19]. We further explore our research to analyze the effect of curcumin on the proteins involved in the ECM remodeling in NE-induced stress in cardiomyocytes.…”

Section: Introductionmentioning

confidence: 99%

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Curcumin Suppresses Gelatinase B Mediated Norepinephrine Induced Stress in H9c2 Cardiomyocytes

et al. 2013

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BackgroundExtracellular matrix (ECM) remodeling facilitates biomechanical signals in response to abnormal physiological conditions. This process is witnessed as one of the major effects of the stress imposed by catecholamines, such as epinephrine and norepinephrine (NE), on cardiac muscle cells. Matrix metalloproteinases (MMPs) are the key proteases involved in degradation of the ECM in heart.ObjectivesThe present study focuses on studying the effect of curcumin on Gelatinase B (MMP-9), an ECM remodeling regulatory enzyme, in NE-induced cardiac stress. Curcumin, a bioactive polyphenol found in the spice turmeric, has been studied for its multi-fold beneficial properties. This study focuses on investigating the role of curcumin as a cardio-protectant.MethodsH9c2 cardiomyocytes were subjected to NE and curcumin treatments to study the response in stress conditions. Effect on total collagen content was studied using Picrosirus red staining. Gelatinase B activity was assessed through Gel-Diffusion Assay and Zymographic techniques. RT-PCR, Western Blotting and Immunocytochemistry were performed to study effect on expression of gelatinase B. Further, the effect of curcumin on the localization of NF-κB, known to regulate gelatinase B, was also examined.ResultsCurcumin suppressed the increase in the total collagen content under hypertrophic stress and was found to inhibit the in-gel and in-situ gelatinolytic activity of gelatinase B. Moreover, it was found to suppress the mRNA and protein expression of gelatinase B.ConclusionsThe study provides an evidence for an overall inhibitory effect of curcumin on Gelatinase B in NE-induced hypertrophic stress in H9c2 cardiomyocytes which may contribute in the prevention of ECM remodeling.

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Section: Resultssupporting

confidence: 80%

Section: Methodsmentioning

confidence: 99%

“…A concentration of 8 µM curcumin as reported earlier by our group was added simultaneous to the NE induction [19]. Cell size was studied and then analyzed by NIH ImageJ.…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Curcumin Suppresses Gelatinase B Mediated Norepinephrine Induced Stress in H9c2 Cardiomyocytes

et al. 2013

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“…A variety of plants and food components have been reported to have beneficial roles in pathological heart diseases. For example, curcumin, quercetin, and resveratrol appear to attenuate myocardial infarction, cardiac hypertrophy [3][4][5], and heart failure [6].…”

Section: Introductionmentioning

confidence: 99%

Piceatannol attenuates cardiac hypertrophy in an animal model through regulation of the expression and binding of the transcription factor GATA binding factor 6

et al. 2014

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a b s t r a c tPiceatannol is found in grapes, passion fruit, and Japanese knotweed. Piceatannol pretreatment suppresses cardiac hypertrophy induced by isoproterenol as assessed by heart weight/body weight ratio, cross-sectional area, and expression of hypertrophic markers. The anti-hypertrophic effect of piceatannol in rat neonatal cardiomyocytes is the same as that in vivo. Piceatannol inhibits lentiviral-GATA6-induced cardiomyocyte hypertrophy. Furthermore, piceatannol reduces the interaction between GATA4 and GATA6 as well as the DNA-binding activity of endogenous GATA6 in the ANP promoter. Our results suggest that piceatannol may be a novel therapeutic agent for the prevention of cardiac hypertrophy. Structured summary of protein interactions:GATA6 physically interacts with GATA4 by anti V5 tag coimmunoprecipitation (View interaction)

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Epigenetics of Aberrant Cardiac Wound Healing

Russell‐Hallinan

Watson

Baugh

2018

Comprehensive Physiology

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Remodeling of cardiac tissue architecture is essential for normal organ development and maintaining homeostasis after injury. Injurious insults to the heart, such as hypertension and myocardial infarction, promote cellular responses including stimulation of resident inflammatory cells, activation of endothelial cells and recruitment of immune cells, hypertrophy of cardiomyocytes, and activation of fibroblasts. The physiological goal of this coordinated cellular response is to repair damaged tissue while maintaining or restoring cardiac contractile function. Persistent uncontrolled inflammation, hypertrophy, and fibrosis in the heart due to hyperactive wound healing are detrimental and impair cardiac performance, facilitating the progression to heart failure. Abnormal changes in gene expression promote acquisition of aberrant cellular phenotypes that drive cardiac remodeling. DNA methylation and histone modifications are epigenetic mechanisms that critically regulate chromatin structure and gene expression, and are essential for normal physiology and development. Increasing clinical and experimental evidence suggests that these epigenetic mechanisms are involved in driving aberrant wound healing and the development of heart failure. While most of our knowledge to date is on the heart as a whole, the precise contribution of DNA methylation and histone modifications in regulating aberrant cardiac remodeling at the cellular level is less defined. Therefore, this overview aims to summarize the role of DNA methylation and histone modifications (acetylation and methylation) in heart failure and to comprehensively dissect the role these mechanisms play in regulating the function of cardiomyocytes, fibroblasts, and immune cells in response to injury. © 2018 American Physiological Society. Compr Physiol 8:451-491, 2018.

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Curcumin: a potential therapeutic polyphenol, prevents noradrenaline-induced hypertrophy in rat cardiac myocytes

Abstract: These findings suggest that curcumin reduces the hypertrophic marker gene expression by inhibiting nuclear localization and DNA binding activity of GATA-4. Thus it has a great anti-hypertrophic potential.

Cited by 28 publications

References 26 publications

Curcumin Suppresses Gelatinase B Mediated Norepinephrine Induced Stress in H9c2 Cardiomyocytes

Curcumin Suppresses Gelatinase B Mediated Norepinephrine Induced Stress in H9c2 Cardiomyocytes

Piceatannol attenuates cardiac hypertrophy in an animal model through regulation of the expression and binding of the transcription factor GATA binding factor 6

Epigenetics of Aberrant Cardiac Wound Healing

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