Resveratrol Ameliorates Cardiac Hypertrophy by Down‐regulation of miR‐155 Through Activation of Breast Cancer Type 1 Susceptibility Protein

Fan, Yuhua; Liu, Li; Fang, Kun; Huang, Tao; Wan, Lin; Liu, Youbin; Zhang, Sen; Yan, Dongxia; Li, Guangnan; Gao, Yanhui; Lv, Yadong; Chen, Yan-Jun; Tu, Yingfeng

doi:10.1161/jaha.115.002648

Cited by 23 publications

(21 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We determined that miR-125a-3p inhibited the expression of BRCA1, a well-known tumor suppressor with multiple interacting partners and diverse biological functions 32 . In contrast, Ucn-1 increased BRCA1 expression under I/R in heart, which may be protective consistent with the role of BRCA1 in regulation of cardiac myocytes survival after myocardial infarction, its shielding of cardiac myocytes from DNA damage 33 , and its prevention of cardiac hypertrophy 34 . miR-125a-3p also reduced significantly the expression of MAP3K12 and XBP1, genes associated with cell stress.…”

Section: Discussionsupporting

confidence: 62%

miR-125a, miR-139 and miR-324 contribute to Urocortin protection against myocardial ischemia-reperfusion injury

Díaz

Calderón-Sánchez

Toro

et al. 2017

Sci Rep

View full text Add to dashboard Cite

Urocortin 1 and 2 (Ucn-1 and Ucn-2) have established protective actions against myocardial ischemia-reperfusion (I/R) injuries. However, little is known about their role in posttranscriptional regulation in the process of cardioprotection. Herein, we investigated whether microRNAs play a role in urocortin-induced cardioprotection. Administration of Ucn-1 and Ucn-2 at the beginning of reperfusion significantly restored cardiac function, as evidenced ex vivo in Langendorff-perfused rat hearts and in vivo in rat subjected to I/R. Experiments using microarray and qRT-PCR determined that the addition of Ucn-1 at reperfusion modulated the expression of several miRNAs with unknown role in cardiac protection. Ucn-1 enhanced the expression of miR-125a-3p, miR-324-3p; meanwhile it decreased miR-139-3p. Similarly, intravenous infusion of Ucn-2 in rat model of I/R mimicked the effect of Ucn-1 on miR-324-3p and miR-139-3p. The effect of Ucn-1 involves the activation of corticotropin-releasing factor receptor-2, Epac2 and ERK1/2. Moreover, the overexpression of miR-125a-3p, miR-324-3p and miR-139-3p promoted dysregulation of genes expression involved in cell death and apoptosis (BRCA1, BIM, STAT2), in cAMP and Ca2+ signaling (PDE4a, CASQ1), in cell stress (NFAT5, XBP1, MAP3K12) and in metabolism (CPT2, FoxO1, MTRF1, TAZ). Altogether, these data unveil a novel role of urocortin in myocardial protection, involving posttranscriptional regulation with miRNAs.

show abstract

Section: Discussionsupporting

confidence: 62%

miR-125a, miR-139 and miR-324 contribute to Urocortin protection against myocardial ischemia-reperfusion injury

Díaz

Calderón-Sánchez

Toro

et al. 2017

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Previous findings from our lab show that Rev protects against cardiomyocytes apoptosis induced by As 2 O 3 through attenuating oxidative stress [18]. In addition, we found that Rev could ameliorate cardiac hypertrophy by attenuation level of miR-155 through activation of Breast Cancer Type 1 Susceptibility Protein (BRCA1) [19]. Recently, Voloshyna et al indicate that Rev could decrease platelet aggregation, induce vasorelaxation, impair endothelial activation, and regulate lipid and lipoprotein metabolism.…”

Section: Introductionmentioning

confidence: 56%

“…6). Findings from our lab and others have demonstrated that Rev possesses various beneficial effects on cardiovascular disease, pulmonary disease, and cancers [19, 32-37]. Jager et al verified that Rev increased the production of serotonin, kynurenine and spermidine, and repressed the level of prostaglandin E2 (PGE2) in the human breast cancer cell lines MCF-7 and MDA-mb-231 [38], indicating that Rev might regulate some small molecules acting as potential markers for disease treatment.…”

Section: Discussionmentioning

confidence: 99%

Metabolomics Reveals Protection of Resveratrol in Diet-Induced Metabolic Risk Factors in Abdominal Muscle

Chen

Zhang

et al. 2018

Cell Physiol Biochem

Self Cite

View full text Add to dashboard Cite

Background/Aims: Abdominal obesity is recognized as the main reason of metabolic syndrome, which is closely related to disordered skeletal and/or abdominal muscle metabolic functions. Metabolomics is a comprehensive assessment system in biological metabolites. The aim of our present study is to investigate the diet-induced metabolic risk factors by metabolic in the abdominal muscles and clarify the relationship between atheroprotective effects of Resveratrol (Rev) and abdominal muscles metabolic components during the development of atherosclerosis. Methods: The mice were randomly divided into three groups including normal group (N), high fat diet (HFD or H) group and high fat diet with Rev treated group (HR). GC-MS combined with pattern recognition approaches were employed to obtain comprehensive metabolic signatures and related differential metabolites after 24 week HFD feeding. Oil Red O staining and Electron microscopy technology (EMT) were employed to detect the size of fatty plaques and intracellular lipid accumulation, respectively. Results: The result indicated that 22 types of metabolites in the abdominal muscles were obviously altered by HFD feeding group. Moreover, Rev treatment obviously increased 11 different kinds of metabolites, most of which were involved in the carbohydrate, amino acid and lipid metabolisms. Importantly, these elevated different metabolites were involved in pathways mainly related to galactose metabolism, alanine, aspartate and glutamate metabolism, glyoxylate and dicarboxylate metabolism in abdominal muscles. Oil Red O staining and Electron microscopy showed less lipid accumulation in the lesions and decreased intracellular lipid deposition in the foam cells in HR group. Conclusions: We concluded that Rev produced a beneficial effect partially by modulating multiple metabolism pathways and metabolites in the abdominal muscles, which may provide a new protective mechanism of Rev on the progression of atherosclerosis. These notably changed metabolites might be potential biomarkers or therapeutic targets during development of metabolic syndrome and atherosclerosis.

show abstract

“…For example, the mice were exposed to bleomycin [30], underwent a transverse aortic constriction (TAC) operation [31], or were fed a controlled diet [32]. Detailed information is presented in Table 9.…”

Section: Discussionmentioning

confidence: 99%

A comparative study of the characterization of miR-155 in knockout mice

Zhang¹,

Cui²,

Li³

et al. 2017

PLoS ONE

View full text Add to dashboard Cite

miR-155 is one of the most important miRNAs and plays a very important role in numerous biological processes. However, few studies have characterized this miRNA in mice under normal physiological conditions. We aimed to characterize miR-155 in vivo by using a comparative analysis. In our study, we compared miR-155 knockout (KO) mice with C57BL/6 wild type (WT) mice in order to characterize miR-155 in mice under normal physiological conditions using many evaluation methods, including a reproductive performance analysis, growth curve, ultrasonic estimation, haematological examination, and histopathological analysis. These analyses showed no significant differences between groups in the main evaluation indices. The growth and development were nearly normal for all mice and did not differ between the control and model groups. Using a comparative analysis and a summary of related studies published in recent years, we found that miR-155 was not essential for normal physiological processes in 8-week-old mice. miR-155 deficiency did not affect the development and growth of naturally ageing mice during the 42 days after birth. Thus, studying the complex biological functions of miR-155 requires the further use of KO mouse models.

show abstract

Resveratrol Ameliorates Cardiac Hypertrophy by Down‐regulation of miR‐155 Through Activation of Breast Cancer Type 1 Susceptibility Protein

Cited by 23 publications

References 36 publications

miR-125a, miR-139 and miR-324 contribute to Urocortin protection against myocardial ischemia-reperfusion injury

miR-125a, miR-139 and miR-324 contribute to Urocortin protection against myocardial ischemia-reperfusion injury

Metabolomics Reveals Protection of Resveratrol in Diet-Induced Metabolic Risk Factors in Abdominal Muscle

A comparative study of the characterization of miR-155 in knockout mice

Contact Info

Product

Resources

About