Combined detection of miR-21-5p, miR-30a-3p, miR-30a-5p, miR-155-5p, miR-216a and miR-217 for screening of early heart failure diseases

Ding, Han; Wang, Yin; Hu, Longgang; Xue, Sheng; Wang, Yu; Zhang, Lei; Zhang, Yuan; Qi, Hongzhao; Yu, Hua; Aung, Lynn Htet Htet; An, Yi; Li, Peifeng

doi:10.1042/bsr20191653

Cited by 32 publications

(25 citation statements)

References 42 publications

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“…Disease Markers miR-216a was positively correlated with the IL1β expression in carotid atherosclerotic plaques, which could give more accurate information about miR-216a as a biomarker for vascular inflammation and atherosclerosis. Additionally, miR-216a is found to be upregulated both in the myocardium tissues and the plasma of heart failure patients compared with healthy controls [17], and the consistent result of plasma miR-216a in heart failure was recently reported by Ding et al [18]. Thus, miR-216a may be a promising biomarker for vascular dysfunctions including endothelial senescence and inflammatory responses, atherosclerotic diseases, and heart failure.…”

supporting

confidence: 67%

MicroRNA-216a Promotes Endothelial Inflammation by Smad7/IκBα Pathway in Atherosclerosis

Yang

Chen

et al. 2020

Disease Markers

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Background. The endothelium is the first line of defence against harmful microenvironment risks, and microRNAs (miRNAs) involved in vascular inflammation may be promising therapeutic targets to modulate atherosclerosis progression. In this study, we aimed to investigate the mechanism by which microRNA-216a (miR-216a) modulated inflammation activation of endothelial cells. Methods. A replicative senescence model of human umbilical vein endothelial cells (HUVECs) was established, and population-doubling levels (PDLs) were defined during passages. PDL8 HUVECs were transfected with miR-216a mimics/inhibitor or small interfering RNA (siRNA) of SMAD family member 7 (Smad7). Real-time PCR and Western blot assays were performed to detect the regulatory role of miR-216a on Smad7 and NF-κB inhibitor alpha (IκBα) expression. The effect of miR-216a on adhesive capability of HUVECs to THP-1 cells was examined. MiR-216a and Smad7 expression in vivo were measured using human carotid atherosclerotic plaques of the patients who underwent carotid endarterectomy ( n = 41 ). Results. Luciferase assays showed that Smad7 was a direct target of miR-216a. Smad7 mRNA expression, negatively correlated with miR-216a during endothelial aging, was downregulated in senescent PDL44 cells, compared with young PDL8 HUVECs. MiR-216a markedly increased endothelial inflammation and adhesive capability to monocytes in PDL8 cells by promoting the phosphorylation and degradation of IκBα and then activating NF-κB signalling pathway. The effect of miR-216a on endothelial cells was consistent with that blocked Smad7 by siRNAs. When inhibiting endogenous miR-216a, the Smad7/IκBα expression was rescued, which led to decreased endothelial inflammation and monocytes recruitment. In human carotid atherosclerotic plaques, Smad7 level was remarkably decreased in high miR-216a group compared with low miR-216a group. Moreover, miR-216a was negatively correlated with Smad7 and IκBα levels and positively correlated with interleukin 1 beta (IL1β) expression in vivo. Conclusion. In summary, our findings suggest a new mechanism of vascular endothelial inflammation involving Smad7/IκBα signalling pathway in atherosclerosis.

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supporting

confidence: 67%

MicroRNA-216a Promotes Endothelial Inflammation by Smad7/IκBα Pathway in Atherosclerosis

Yang

Chen

et al. 2020

Disease Markers

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“…in this study, it was found that Hdac2-mediated H3K14 hyperacetylation contributed to mir-30a-5p upregulation in HPostc. in recent years, accumulating evidence has demonstrated that mir-30a-5p participates in cardiovascular pathophysiology (39)(40)(41). although several studies have indicated the importance of mir-30a-5p in cardiovascular diseases, there are still conflicting views.…”

Section: Discussionmentioning

confidence: 99%

H3K14 hyperacetylation‑mediated c‑Myc binding to the miR‑30a‑5p gene promoter under hypoxia postconditioning protects senescent cardiomyocytes from hypoxia/reoxygenation injury

Zhang

Wang

et al. 2021

Mol Med Rep

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our previous study reported that microrna (mir)-30a-5p upregulation under hypoxia postconditioning (HPostc) exert a protective effect on aged H9c2 cells against hypoxia/reoxygenation injury via dna methyltransferase 3B-induced dna hypomethylation at the mir-30a-5p gene promoter. This suggests that mir-30a-5p may be a potential preventative and therapeutic target for ischemic heart disease in aged myocardium. The present study aimed to investigate the underlying mechanisms of mir-30a-5p transcription in aged myocardium in ischemic heart disease. cardiomyocytes were treated with 8 mg/ml d-galactose for 9 days, and then exposed to hypoxic conditions. cell viability was determined using a cell viability assay. expression levels of histone deacetylase 2 (Hdac2), lc3B-ii/i, beclin-1 and p62 were detected via reverse transcription-quantitative Pcr and western blotting. chromatin immunoprecipitation-Pcr and luciferase reporter assays were performed to evaluate the effect of c-Myc binding and activity on the mir-30a-5p promoter in senescent cardiomyocytes following HPostc. it was found that HPostc enhanced the acetylation levels of H3K14 at the mir-30a-5p gene promoter in senescent cardiomyocytes, which attributed to the decreased expression of Hdac2. in addition, c-Myc could positively regulate mir-30a-5p transcription to inhibit senescent cardiomyocyte autophagy. Mechanically, it was observed that increased H3K14 acetylation level exposed to romidepsin facilitated c-Myc binding to the mir-30a-5p gene promoter region, which led to the increased transcription of mir-30a-5p. Taken together, these results demonstrated that Hdac2-mediated H3K14 hyperacetylation promoted c-Myc binding to the mir-30a-5p gene promoter, which contributed to HPostc senescent cardioprotection.

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“…The included studies were published between 2007 and 2021. Twenty-three studies were conducted in China [ 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 ]; ten in the United States [ 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 ]; five in Iran [ 47 , 48 , 49 , 50 , 51 ]; four in Italy [ 52 , 53 , 54 , 55 ]; three in the Netherlands [ 56 , 57 , 58 ]; three in Germany [ 59 , 60 , 61 ]; two in Taiwan [ 62 , 63 ]; two in Australia [ 64 , 65 ]; and one each in New Zealand [ 66 …”

Section: Resultsmentioning

confidence: 99%

“…The included studies assessed different genetic components. Twenty-four studies involved the assessment of single-nucleotide polymorphism (SNP) [ 18 , 19 , 20 , 21 , 26 , 28 , 33 , 39 , 40 , 42 , 43 , 45 , 47 , 48 , 49 , 50 , 51 , 52 , 62 , 63 , 67 , 69 , 72 , 74 ], eight studies were on the transcriptome [ 23 , 29 , 36 , 41 , 46 , 54 , 61 , 71 ], twenty-three studied microRNA (miRNA) [ 14 , 15 , 16 , 22 , 23 , 24 , 29 , 30 , 31 , 32 , 37 , 38 , 44 , 55 , 56 , 57 , 58 , 61 , 65 , 66 , 68 , …”

Section: Resultsmentioning

confidence: 99%

“…Twenty-three of the included studies reported the changes of miRNA in HF [ 14 , 15 , 16 , 22 , 23 , 24 , 29 , 30 , 31 , 32 , 37 , 38 , 44 , 55 , 56 , 57 , 58 , 61 , 65 , 66 , 68 , 71 , 73 ]. All of them examined the outcome in peripheral blood except one, which examined the miRNA changes in cardiac tissue only [ 61 ].…”

Section: Resultsmentioning

confidence: 99%

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Exploration of Potential Genetic Biomarkers for Heart Failure: A Systematic Review

Chan

Waye

Liu

et al. 2021

IJERPH

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Patients with heart failure (HF) often present with signs and symptoms that are often nonspecific and with a wide differential diagnosis, making diagnosis and prognosis of HF by clinical presentation alone challenging. Our knowledge on genetic diversity is rapidly evolving with high-throughput DNA sequencing technology, which makes a great potential for genetic biomarker development. The present review attempts to provide a comprehensive review on the modification of major genetic components in HF patients and to explore the potential application of these components as clinical biomarkers in the diagnosis and in monitoring the progress of HF. The literature search was conducted using six databases, resulting in the inclusion of eighteen studies in the review. The findings of these studies were summarized narratively. An appraisal of the reporting quality of the included studies was conducted using a twelve-item checklist adapted from the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) checklist. The findings showed that changes in genetic components in patients with HF compared to healthy controls could be noninvasive diagnostic or prognostic tools for HF with higher specificity and sensitivity in comparison with the traditional biomarkers. This review provided evidence for the potential of developing genetic biomarkers of HF.

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Combined detection of miR-21-5p, miR-30a-3p, miR-30a-5p, miR-155-5p, miR-216a and miR-217 for screening of early heart failure diseases

Cited by 32 publications

References 42 publications

MicroRNA-216a Promotes Endothelial Inflammation by Smad7/IκBα Pathway in Atherosclerosis

MicroRNA-216a Promotes Endothelial Inflammation by Smad7/IκBα Pathway in Atherosclerosis

H3K14 hyperacetylation‑mediated c‑Myc binding to the miR‑30a‑5p gene promoter under hypoxia postconditioning protects senescent cardiomyocytes from hypoxia/reoxygenation injury

Exploration of Potential Genetic Biomarkers for Heart Failure: A Systematic Review

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