Gallic acid attenuates calcium calmodulin‐dependent kinase <scp>II</scp>‐induced apoptosis in spontaneously hypertensive rats

Jin, Li; Piao, Zhe; Liu, Chun Ping; Sun, Simei; Liu, Bin; Kim, Gwi Ran; Choi, Sin Young; Ryu, Yuhee; Kee, Hae Jin; Cho, Jeong Gwan

doi:10.1111/jcmm.13419

Cited by 22 publications

(17 citation statements)

References 41 publications

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“…Wheat germ agglutinin (WGA) staining was performed to show the contour and measure of cardiomyocyte size. 22,23 As shown in Taken together, these results suggested that knockdown of ln-cRNA MEG3 could inhibit cardiomyocyte hypertrophy, cardiomyocyte loss and cardiac fibrosis in the border zone following MI.…”

Section: The Effects Of Lncrna Meg3 Knockdown On Myocardial Infarctsupporting

confidence: 54%

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Long non‐coding RNA MEG3 knockdown attenuates endoplasmic reticulum stress‐mediated apoptosis by targeting p53 following myocardial infarction

Zhao

Chen

et al. 2019

J Cellular Molecular Medi

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Mounting evidence has indicated that long non‐coding RNA maternally expressed gene 3 (lncRNA MEG3) regulates cell apoptosis, and is involved in a variety of diseases. However, its exact role in myocardial infarction (MI) has not been fully elucidated. In the present study, we firstly observed that the expression levels of the lncRNA MEG3 in infarct hearts and hypoxic neonatal mice ventricular myocytes (NMVMs) were up‐regulated by quantitative real‐time PCR (qRT‐PCR). Then, we knocked down lncRNA MEG3 by lentiviral delivery in the myocardial border region following multipoint injection. Following 28 days of MI, the lncRNA MEG3 knockdown mice indicated better cardiac function, and less cardiac remodelling by ultrasonic cardiogram and histological analysis. In addition, we indicated that lncRNA MEG3 knockdown reduced myocyte apoptosis and reactive oxygen species production in MI mice model and hypoxic NMVMs. Furthermore, we revealed that knockdown of lncRNA MEG3 protected against endoplasmic reticulum stress (ERS)‐mediated myocardial apoptosis including the induction of PERK‐eIF2α and caspase 12 pathways. At last, we provided evidence that p53 was identified as a protein target of lncRNA MEG3 to regulate NF‐κB‐ and ERS‐associated apoptosis. Taken collectively, our findings demonstrated that lncRNA MEG3 knockdown exerted cardioprotection by reducing ERS‐mediated apoptosis through targeting p53 post‐MI.

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Section: The Effects Of Lncrna Meg3 Knockdown On Myocardial Infarctsupporting

confidence: 54%

“…Wheat germ agglutinin (WGA) staining was performed to show the contour and measure of cardiomyocyte size . As shown in Figure C, the staining results indicated that the hearts from MI group exhibited enlarged cardiomyocyte size and reduced cardiomyocyte number in border zone compared with those of the sham group at 4 weeks post‐MI.…”

Section: Resultsmentioning

confidence: 99%

Long non‐coding RNA MEG3 knockdown attenuates endoplasmic reticulum stress‐mediated apoptosis by targeting p53 following myocardial infarction

Zhao

Chen

et al. 2019

J Cellular Molecular Medi

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“…Gallic acid (GA) is a natural phenolic acid that is abundant in several plants. Accumulating evidence has demonstrated that GA plays a beneficial role in apoptosis, hypertension, cardiac hypertrophy, and fibrosis ( Ryu et al, 2016 ; Jin et al, 2017 , 2018a , b ). GA improved isoproterenol-induced cardiomyocyte hypertrophy and fibrosis by inhibiting the JNK2-Smad3 signaling pathway ( Ryu et al, 2016 ).…”

Section: Introductionmentioning

confidence: 99%

Gallic Acid Ameliorates Angiotensin II-Induced Atrial Fibrillation by Inhibiting Immunoproteasome- Mediated PTEN Degradation in Mice

Han

Zhang

et al. 2020

Front. Cell Dev. Biol.

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Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia and is a major cause of stroke and heart failure. We and others have found that gallic acid (GA) plays a beneficial role in cardiac hypertrophic remodeling and hypertension. However, the effect of GA on angiotensin II (Ang II)-induced AF and atrial remodeling as well as the underlying mechanisms remain unknown. AF was induced in mice by Ang II infusion (2000 ng/kg/min) for 3 weeks. Blood pressure was measured using the tail-cuff method. Atrial volume was evaluated by echocardiography. Atrial remodeling was studied using hematoxylin and eosin, Masson’s trichrome, and immunohistochemical staining. Atrial oxidative stress was assessed by dihydroethidium staining. The gene expression of fibrotic and inflammatory markers and protein levels of signaling mediators were measured by quantitative real-time PCR and western blot analysis. In mice, GA administration significantly attenuated Ang II-induced elevation of blood pressure, AF incidence and duration, atrial dilation, fibrosis, inflammation, and oxidative stress compared with the vehicle control. Furthermore, GA downregulated Ang II-induced activity and expression of immunoproteasome subunits (β2i and β5i), which reduced PTEN degradation and led to the inactivation of AKT1 and downstream signaling mediators. Importantly, blocking PTEN activity by VO-Ohpic markedly reversed the GA-mediated protective effects on Ang II-induced AF and atrial remodeling. Therefore, our results provide novel evidence that GA exerts a cardioprotective role by inhibiting immunoproteasome activity, which attenuates PTEN degradation and activation of downstream signaling, and may represent a promising candidate for treating hypertensive AF.

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“…To investigate lung histological changes resulting from heart failure and acute toxicity, paraffin-embedded tissues were cut transversely into 3-µm-thick sections, deparaffinized with xylene, and then rehydrated with different grades of alcohol before staining with H&E, as previously described 22 . Photomicrographs were obtained using an Eclipse Ti-U microscope (Nikon, Tokyo, Japan).…”

Section: Methodsmentioning

confidence: 99%

Gentisic acid prevents the transition from pressure overload-induced cardiac hypertrophy to heart failure

Sun

Kee

Ryu

et al. 2019

Sci Rep

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We previously reported that gentisic acid attenuates cardiac hypertrophy and fibrosis in transverse aortic constriction (TAC)-induced cardiac hypertrophy. Here, we examined whether gentisic acid prevents the development of heart failure. Heart failure was induced in mice via chronic TAC. Mice were administered the vehicle, gentisic acid (10 and 100 mg∙kg −1 ∙day −1 ), or bisoprolol (0.5 mg∙kg −1 ∙day −1 ) orally for 3 weeks, beginning 3 weeks after TAC. After oral administration of gentisic acid (2000 mg∙kg −1 ), no significant differences in organ weight, histology, or analyzed serum and hematological parameters were observed between female mice in the control and gentisic acid-treated groups. Gentisic acid administration inhibited cardiac dysfunction in a dose-dependent manner, and reduced cardiac hypertrophy and fibrosis, as was revealed via western blotting, quantitative real-time PCR, and Masson’s trichrome staining. Gentisic acid dose-dependently reduced the expression of fibrosis marker genes, suppressed the renin-angiotensin-aldosterone system, and reduced lung size and pulmonary vascular remodeling. Our data indicate that gentisic acid prevents cardiac hypertrophy, fibrosis, cardiac dysfunction, and pulmonary pathology in TAC-induced heart failure. These findings suggest that supplementation with gentisic acid may provide an advantage in preventing the progression from cardiac hypertrophy to heart failure.

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Gallic acid attenuates calcium calmodulin‐dependent kinase II‐induced apoptosis in spontaneously hypertensive rats

Cited by 22 publications

References 41 publications

Long non‐coding RNA MEG3 knockdown attenuates endoplasmic reticulum stress‐mediated apoptosis by targeting p53 following myocardial infarction

Long non‐coding RNA MEG3 knockdown attenuates endoplasmic reticulum stress‐mediated apoptosis by targeting p53 following myocardial infarction

Gallic Acid Ameliorates Angiotensin II-Induced Atrial Fibrillation by Inhibiting Immunoproteasome- Mediated PTEN Degradation in Mice

Gentisic acid prevents the transition from pressure overload-induced cardiac hypertrophy to heart failure

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