Ellagic acid promotes ventricular remodeling after acute myocardial infarction by up-regulating miR-140-3p

Wei, Dazhen; Lin, Cong; Huang, Yinqing; Wu, Lianpin; Huang, Ming-Yuan

doi:10.1016/j.biopha.2017.07.106

Cited by 27 publications

(13 citation statements)

References 22 publications

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“…Also, oral pretreatment with ellagic acid restored pathological arrhythmias in MI rats (Kannan and Quine, 2013). Further, our previous study indicated that ellagic acid improved ventricular remodeling after MI by regulating the miR-140-3p/ MKK6 pathway (Wei et al, 2017). Similarly, we found that ellagic acid decreased expression of fibrosis-related factor in MI rats, reduced the area of cardiac fibrosis and inhibited the proliferation and migration of CFs.…”

Section: Discussionsupporting

confidence: 54%

“…Recent studies observed the vital function of ellagic acid in protecting cardiovascular system. For example, ellagic acid could reduce the area of MI and suppress cardiac fibrosis by regulating the expression of anti-apoptosis genes and enhancing activities of mitochondrial respiratory enzymes (Mari Kannan and Darlin Quine, 2012;Wei et al, 2017). Furthermore, the occurrence of ventricular hypertrophy could be decreased by ellagic acid via the suppression of lipid peroxidation (Kannan and Quine, 2013).…”

Section: Introductionmentioning

confidence: 99%

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Ellagic acid inhibits proliferation and migration of cardiac fibroblasts by down-regulating expression of HDAC1

et al. 2019

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Cardiac fibroblasts (CFs) could be activated after myocardial infarction (MI). Thus, it is necessary to explore effective drugs to suppress the activation of CFs following MI. This study was designed to investigate the impacts of ellagic acid on CFs and the underlying mechanisms. The expression of histone deacetylases (HDACs) and fibrosis-related genes was detected by qRT-PCR and western blot. The Masson's Trichrome Staining assay was used to evaluate the area of cardiac fibrosis. The proliferation and migration of CFs were measured by CCK8 Kit and Transwell assay, respectively. Our results showed that ellagic acid significantly reduced protein expression of HDAC1, mRNA expression of collagen I, collagen III, MMP-2 and MMP-9 and the area of cardiac fibrosis in MI rats. In Ang II-stimulated CFs, ellagic acid (60 μmol/L) decreased the protein expression of HDAC1, collagen I, collagen III, MMP-2 and MMP-9, and inhibited cell proliferation and migration. Further, HDAC1 over-expression reversed the inhibitor effects of ellagic acid on proteins expression (collagen I, collagen III, MMP-2 and MMP-9) and proliferation and migration of CFs. The present results suggested that ellagic acid suppressed proliferation and migration of CFs by down-regulating expression of HDAC1.

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Section: Discussionsupporting

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Ellagic acid inhibits proliferation and migration of cardiac fibroblasts by down-regulating expression of HDAC1

et al. 2019

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“…The present results demonstrated that ox-LDL significantly downregulated miR-140-3p expression in a time-dependent manner. A recent study demonstrated that ellagic acid could upregulate miR-140-3p expression and inhibit MAP kinase kinase 6 expression to inhibit apoptosis in cardiomyocytes (29). However, little is known regarding the role of miR-140-3p in the apoptosis of HUVECs.…”

Section: Discussionmentioning

confidence: 99%

Astragaloside IV inhibits oxidized low‑density lipoprotein‑induced endothelial damage via upregulation of miR‑140‑3p

Qian

Cai

et al. 2019

Int J Mol Med

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Oxidized low-density lipoprotein (ox-LdL)-mediated endothelial cell injury has an important role in the vascular complications of type 2 diabetes. Astragaloside IV (ASV) is an active component of Radix Astragali, which has been demonstrated to exert protective effects against endothelial damage. The present study explored whether microRNAs (miRNAs) are involved in mediating the protective effects of ASV on ox-LdL-induced damage in human umbilical vein endothelial cells (HUVEcs). RNA sequencing and reverse transcription-quantitative PcR analyses revealed that ox-LdL treatment significantly downregulated miR-140-3p expression in HUVECs. miR-140-3p overexpression promoted cell proliferation and inhibited apoptosis in ox-LdL-induced HUVEcs. However, inhibition of miR-140-3p expression could reverse the effects of ASV on ox-LdL-induced HUVEcs and reactivate ASV-inhibited PI3K/Akt signaling in ox-LdL-induced HUVECs. In addition, Krüppel-like factor 4 (KLF4) was identified as a target of miR-140-3p in ox-LDL-treated HUVECs. Subsequent experiments revealed that KLF4 overexpression partially counteracted the protective effects of miR-140-3p or ASV treatment in ox-LdL-induced HUVEcs. Taken together, the current findings demonstrated that the protective effects of ASV on HUVECs were dependent on miR-140-3p upregulation and subsequent inhibition of KLF4 expression, which in turn suppressed the PI3K/Akt signaling pathway. The present results shed light to the molecular mechanism by which ASV alleviated ox-LdL-induced endothelial cell damage.

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“…Ellagic acid decreases endothelial ROS level and vascular oxidative stress, and ameliorates vascular relaxation impairment through modulation of the ERK1/2/NOX4 signalling pathway (Rozentsvit et al, 2017). Also, in 2017, ellagic acid improved ventricular remodelling following myocardial infarction by up-regulating miR-140-3p expression and inhibiting MKK6 expression (Wei et al, 2017). In a Nω-Nitro-L-arginine methyl ester hydrochloride-induced hypertension model, ellagic acid improved blood pressure, possibly through improving NO bioavailability.…”

Section: Ellagic Acidmentioning

confidence: 99%

Implication of dietary phenolic acids on inflammation in cardiovascular disease

Ali

Ahmad

Budin

et al. 2020

Reviews in Cardiovascular Medicine

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Ellagic acid promotes ventricular remodeling after acute myocardial infarction by up-regulating miR-140-3p

Cited by 27 publications

References 22 publications

Ellagic acid inhibits proliferation and migration of cardiac fibroblasts by down-regulating expression of HDAC1

Ellagic acid inhibits proliferation and migration of cardiac fibroblasts by down-regulating expression of HDAC1

Astragaloside IV inhibits oxidized low‑density lipoprotein‑induced endothelial damage via upregulation of miR‑140‑3p

Implication of dietary phenolic acids on inflammation in cardiovascular disease

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