Differential Regulation of MicroRNAs in End-Stage Failing Hearts Is Associated with Left Ventricular Assist Device Unloading

Barsanti, Cristina; Trivella, Maria Giovanna; D’Aurizio, Romina; Baroudi, Mariama El; Baumgart, Mario; Groth, Marco; Caruso, Raffaele; Verde, Alessandro; Botta, Luca; Cozzi, Lorena; Pitto, Letizia

doi:10.1155/2015/592512

Cited by 37 publications

(25 citation statements)

References 43 publications

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“…Accumulating evidence suggests that miR-142-5p is hematopoietic-specific in the circulation [15][16][17]. It is a key regulator in macrophage apoptosis, cardiac hypertrophy, atherosclerosis, and heart failure [18][19][20]. Platelet extracellular vesicles exhibit upregulated miR-142-5p, which is involved in vascular and metabolic disease [21].…”

Section: Discussionmentioning

confidence: 99%

“…miR-142-5p was upregulated in heart failure patients undergoing implantation of a left ventricular assisting device. The identified miRNAs may contribute to the molecular regulation of reverse remodeling and heart recovery mechanisms [20]. The inhibition of miR-142-5p attenuated OGD/R-induced cell injury and oxidative stress, and overexpression of miR-142-5p aggravated these conditions [23].…”

Section: Discussionmentioning

confidence: 99%

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Plasma miR-142 predicts major adverse cardiovascular events as an intermediate biomarker of dual antiplatelet therapy

Tang

Lei

et al. 2018

Acta Pharmacol Sin

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MicroRNAs (miRNAs) are widely expressed in organisms and are implicated in the regulation of most biological functions. The present study investigated the association of plasma miRNAs with the clinical outcomes of dual antiplatelet therapy in coronary artery disease (CAD) patients who underwent percutaneous coronary intervention (PCI). Plasma miRNA levels were screened using high-throughput Illumina sequencing to evaluate the antiplatelet efficacy of clopidogrel and aspirin. Six plasma miRNAs (miR-126, miR-130a, miR-27a, miR-106a, miR-21, and miR-142) were associated with clopidogrel-treated platelet aggregation. These miRNAs were validated in a prospective cohort of 1230 CAD patients using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). High plasma miR-142 levels were associated with a high risk of major adverse cardiovascular events (MACE), with a hazard ratio (95% confidence interval) of 1.83 (1.30-2.59) at a false discovery rate of <5%. Multivariable Cox regression analysis revealed that diabetes mellitus, heart failure, calcium channel blocker application, and a high plasma miR-142 level were independent risk factors of MACE. The levels of the six plasma miRNAs were not significantly associated with bleeding events during the 3-year follow-up. In conclusion, plasma miR-142 is potential marker to predict MACE in CAD patients after PCI.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Plasma miR-142 predicts major adverse cardiovascular events as an intermediate biomarker of dual antiplatelet therapy

Tang

Lei

et al. 2018

Acta Pharmacol Sin

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“…Moreover, miR-200b-3p is sensitive to hypoxia and is involved in the induction of angiogenesis by directly targeting Ets-1 [41]. On the other hand, miR-338-3p is correlated with off-pump cardiac index values in transplanted hearts of heart failure patients with left ventricular assist device (LVAD) assistance when compared to those without LVAD assistance [42]. These miRNAs play important roles for the heart in the initial phase of hypoxia by targeting their respective targets.…”

Section: Discussionmentioning

confidence: 99%

δ-Opioid Receptor Activation and MicroRNA Expression in the Rat Heart Under Prolonged Hypoxia

Zhi

Li²,

Shao³

et al. 2016

Cell Physiol Biochem

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Background: Hypoxic/ischemic injury to the heart is a frequently encountered clinical problem with limited therapeutic options. Since microRNAs (miRNAs) are involved in hypoxic/ischemic events, and δ-opioid receptor (DOR) activation is known to protect against hypoxic/ischemic injury, we speculated on the involvement of DOR activation in altering miRNA expression in the heart under hypoxic conditions. The present study aimed to test our hypothesis. Methods: Male Sprague Dawley rats were exposed to hypoxia (9.5-10% O₂) for 1, 5, or 10 days with or without DOR activation. The target miRNAs were selected from TaqMan low-density array (TLDA) data and were further analyzed by quantitative real-time PCR. Results: We found that: 1) hypoxia alters the miRNA expression profiles depending on the hypoxic duration; 2) DOR activation shifts miRNA expression profiles in normoxic conditions and upregulates miR-128a-3p, miR-134-5p, miR-135a, miR-193a-3p, miR-196a, miR-324-3p, and miR-338; and 3) DOR activation modifies hypoxia-induced changes in miRNA expression and increases the levels of miR-128a-3p, miR-134-5p, miR-135a, miR-193a-3p, miR-196a, miR-324-3p, miR-141, miR-200b, and miR-324-3p. For example, miR-196c-5p decreased by 50% while miR-135a-5p increased 2.9 fold after 10 days under hypoxic conditions. Moreover, DOR activation further strengthened the hypoxia-induced increase of the levels of miR-7a-5p. When DOR was activated using UFP-512, the level of miR-107-3p significantly increased 1 day after the administration of UFP-512, but gradually decreased back to normal under normoxia. Conclusion: Hypoxia significantly modifies the miRNA profile in the heart, which can be mimicked or modified by DOR activation. Defining the targeted pathways that regulate the diverse cellular and molecular functions of miRNAs may provide new insights into potential therapies for hypoxic/ischemic injury of the heart.

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“…Mansego et al (27) found that miR-216a-5p might be involved in miRNA mediated epigenetic regulation in childhood obesity and the coding regions of miR-216a-5p were methylated (27). Furthermore, it was suggested that miR-216a-5p had an impact on chronic kidney diseases (28), nephrotic syndrome (29) and end-stage failing hearts (30).…”

Section: Discussionmentioning

confidence: 99%

miR-216a-5p acts as an oncogene in renal cell carcinoma

et al. 2018

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Abstract. MiR-216a-5p has been acknowledged as an oncogene and is known to be involved in the progression and metastasis of numerous cancer subtypes. However, the potential role of miR-216a-5p in renal cell carcinoma (RCC) remains to be elucidated. In the present study, reverse transcription-quantitative polymerase chain reaction was performed to detect the expression levels of miR-216a-5p in RCC tissues. Cell counting kit-8, MTT, wound scratch, Transwell and flow cytometric assays were performed to establish the biological functions of miR-216a-5p in RCC. Functional experiments demonstrated that the expression of miR-216a-5p was upregulated in RCC (P<0.05) and miR-216a-5p mimics promoted cellular proliferation, viability and motility, and suppressed apoptosis. Conversely, miR-216a-5p inhibitor suppressed cellular proliferation, viability, motility and induced apoptosis. Based on these findings, it was concluded that miR-216a-5p may function as an oncogene in RCC. MiR-216a-5p target genes need to be explored and the potential of miR-216a-5p to be used as a diagnostic or a prognostic biomarker for RCC needs to be validated by future research.

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Differential Regulation of MicroRNAs in End-Stage Failing Hearts Is Associated with Left Ventricular Assist Device Unloading

Cited by 37 publications

References 43 publications

Plasma miR-142 predicts major adverse cardiovascular events as an intermediate biomarker of dual antiplatelet therapy

Plasma miR-142 predicts major adverse cardiovascular events as an intermediate biomarker of dual antiplatelet therapy

δ-Opioid Receptor Activation and MicroRNA Expression in the Rat Heart Under Prolonged Hypoxia

miR-216a-5p acts as an oncogene in renal cell carcinoma

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