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

Kee, Hae Jin; Park, Sangha; Kang, Woo Dae; Lim, Kyung Seob; Kim, Jung Ha; Ahn, Youngkeun; Jeong, Myung Ho

doi:10.1016/j.febslet.2014.03.027

Cited by 15 publications

(10 citation statements)

References 20 publications

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“…Primary rat neonatal cardiomyocytes were prepared from the hearts of 2-day-old Sprague-Dawley rats (Orient Bio, South Korea) as described previously 22 . Briefly, after euthanasia by decapitation, heart tissues were cut and digested with enzymatic solution (collagenase type II and pancreatin).…”

Section: Methodsmentioning

confidence: 99%

“…Recent studies have shown that phytochemicals including flavonoid, quercetin, curcumin, and resveratrol ameliorate left ventricular hypertrophy in vivo and in vitro 17 18 19 20 . In addition, our group has reported that pretreatment with sulforaphane or piceatannol prevents cardiac hypertrophy through regulation of transcription factor GATA4 or GATA6 21 22 . These evidences indicate the potential of phytochemicals as therapeutics for pathological diseases.…”

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confidence: 99%

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Gallic acid prevents isoproterenol-induced cardiac hypertrophy and fibrosis through regulation of JNK2 signaling and Smad3 binding activity

Ryu

Jin

Kee

et al. 2016

Sci Rep

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Gallic acid, a type of phenolic acid, has been shown to have beneficial effects in inflammation, vascular calcification, and metabolic diseases. The present study was aimed at determining the effect and regulatory mechanism of gallic acid in cardiac hypertrophy and fibrosis. Cardiac hypertrophy was induced by isoproterenol (ISP) in mice and primary neonatal cardiomyocytes. Gallic acid pretreatment attenuated concentric cardiac hypertrophy. It downregulated the expression of atrial natriuretic peptide, brain natriuretic peptide, and beta-myosin heavy chain in vivo and in vitro. Moreover, it prevented interstitial collagen deposition and expression of fibrosis-associated genes. Upregulation of collagen type I by Smad3 overexpression was observed in cardiac myoblast H9c2 cells but not in cardiac fibroblasts. Gallic acid reduced the DNA binding activity of phosphorylated Smad3 in Smad binding sites of collagen type I promoter in rat cardiac fibroblasts. Furthermore, it decreased the ISP-induced phosphorylation of c-Jun N-terminal kinase (JNK) and extracellular signal regulated kinase (ERK) protein in mice. JNK2 overexpression reduced collagen type I and Smad3 expression as well as GATA4 expression in H9c2 cells and cardiac fibroblasts. Gallic acid might be a novel therapeutic agent for the prevention of cardiac hypertrophy and fibrosis by regulating the JNK2 and Smad3 signaling pathway.

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Section: Methodsmentioning

confidence: 99%

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confidence: 99%

Gallic acid prevents isoproterenol-induced cardiac hypertrophy and fibrosis through regulation of JNK2 signaling and Smad3 binding activity

Ryu

Jin

Kee

et al. 2016

Sci Rep

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“…Since these molecules are generally non toxic and well tolerated in vivo, they may represent an interesting alternative to the currently antileishmanial therapy (Baur and Sinclair, 2006;Kee et al, 2014;Li et al, 2014). In a previous work, we studied a series of cis-and trans-resveratrol bearing 3,5-dimetoxy motif at the A phenyl ring and amino, methoxy and hydroxyl function at 3 0 -and/or 4 0 -position.…”

Section: Discussionmentioning

confidence: 99%

In vitro antileishmanial activity of trans-stilbene and terphenyl compounds

Castelli

Bruno

Vitale

et al. 2016

Experimental Parasitology

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h i g h l i g h t s g r a p h i c a l a b s t r a c tWe evaluated the leishmanicidal activity of a pool of new stilbene and terphenyl derivatives. Therphenyl 11 showed a leshmanicidal activity higher than pentostam and TTAS. Therphenyl 11 induces apoptosis in Leishmania parasites while saving macrophages and normal cells. Currently available drugs present different drawbacks, so there is an urgent need to develop new, safe and cost-effective drugs against leishmaniasis. In this study we tested a small library of trans-stilbene and terphenyl derivatives against promastigote, amastigotes and intramacrophage amastigote forms of Leishmania infantum. Two compounds of the series, the trans-stilbene 3 and the terphenyl 11, presented the best activity and safety profiles. Terphenyl 11 showed a leshmanicidal activity higher than pentostam and the ability to induce apoptosis selectively in Leishmania infantum while saving macrophages and primary epithelial cells. Our data indicate that terphenyl compounds, as well as stilbenes, are endowed with leishmanicidal activity, showing potential for further studies in the context of leishmanial therapy.

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“…Primary rat neonatal cardiomyocytes were isolated from 2-day-old Sprague-Dawley rat heart as reported previously [9]. Rat cardiac H9C2 cells purchased from ATCC were cultured in DMEM media supplemented with 10% fetal calf serum and 100U/ml penicillin/streptomycin (Gibco).…”

Section: Methodsmentioning

confidence: 99%

Caspase-Independent Pathway is Related to Nilotinib Cytotoxicity in Cultured Cardiomyocytes

Yang

Zhang

Wang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Cardiotoxicity is a predominant side-effect of nilotinib during chronic myeloid leukemia treatment. The underlying molecular mechanism remains unclear. The role of autophagy and mitochondrial signaling was investigated in nilotinib-treated cardiac H9C2 cells. Methods: Cytotoxicity was assessed using Cell Death Detection kit. Immunoblot and immunofluorescence staining was performed, and cathepsin B and caspase3 activity was assessed in nilotinib-treated H9C2 cells with or without distinct pathway inhibitor or specific siRNA. Results: Nilotinib time- and dose-dependently induced H9C2 apoptosis, which was not completely prevented by the pan caspase inhibitor z-VAD-fmk. Following nilotinib treatment, mitochondrial membrane potential decreased significantly accompanied with remarkable morphological changes. Nuclear translocation of mitochondrial apoptosis inducing factor (AIF) and increased p53 was detected in nilotinib-treated cells. AIF knockdown prevented nilotinib-induced increase of p53 and apoptosis. Additionally, increased cathepsin B activity was detected, and inhibition of cathepsin B by CA-074Me prevented nilotinib-induced apoptosis and nuclear translocation of AIF. Moreover, increased Atg5 and transition of LC3-I to LC3-II was revealed following nilotinib treatment. Increased cathepsin B activity and apoptosis by nilotinib was significantly prohibited by specific autophagy inhibitor bafilomycin A and Atg5 knockdown. Conclusion: Our findings demonstrate that nilotinib increases autophagy and cathepsin B activity, leading to mitochondrial AIF release and nuclear translocation, which is responsible for p53 and apoptosis induction in H9C2 cells.

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

Cited by 15 publications

References 20 publications

Gallic acid prevents isoproterenol-induced cardiac hypertrophy and fibrosis through regulation of JNK2 signaling and Smad3 binding activity

Gallic acid prevents isoproterenol-induced cardiac hypertrophy and fibrosis through regulation of JNK2 signaling and Smad3 binding activity

In vitro antileishmanial activity of trans-stilbene and terphenyl compounds

Caspase-Independent Pathway is Related to Nilotinib Cytotoxicity in Cultured Cardiomyocytes

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