The relevance of microRNA in post-infarction left ventricular remodelling and heart failure

Dutka, Mieczysław; Bobiński, Rafał; Korbecki, Jan

doi:10.1007/s10741-019-09770-9

Cited by 30 publications

(33 citation statements)

References 70 publications

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“…Among the four TIMPs, Timp3 has the longest 3' untranslated region (UTR) contained in the exon 5 (Leco et al, 1994;Apte et al, 1995), which is a target for multiple microRNAs. MicroRNAs (miRNA, miR) are a group of short, non-coding RNAs with 18−25 bases which can regulate gene expression at the transcriptional and post-transcriptional stages (Mohr and Mott, 2015;Dutka et al, 2019;Yao et al, 2019). MiRNAs have been shown widely to be involved in cardiovascular diseases (Barwari et al, 2016;De Rosa et al, 2017;Kir et al, 2018;Dutka et al, 2019).…”

Section: Micrornas Bind To and Downregulate Timp3mentioning

confidence: 99%

“…MicroRNAs (miRNA, miR) are a group of short, non-coding RNAs with 18−25 bases which can regulate gene expression at the transcriptional and post-transcriptional stages (Mohr and Mott, 2015;Dutka et al, 2019;Yao et al, 2019). MiRNAs have been shown widely to be involved in cardiovascular diseases (Barwari et al, 2016;De Rosa et al, 2017;Kir et al, 2018;Dutka et al, 2019). MiR-17-92 cluster is able to induce cardiomyocyte proliferation in postnatal and adult heart as well as in response to myocardial infarction (Chen et al, 2013), which is partly caused by binding of miR-17 to 3' UTR of Timp3 and suppressing Timp3 expression (Shi et al, 2017;Liu et al, 2018).…”

Section: Micrornas Bind To and Downregulate Timp3mentioning

confidence: 99%

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Biology of Tissue Inhibitor of Metalloproteinase 3 (TIMP3), and Its Therapeutic Implications in Cardiovascular Pathology

Fan

Kassiri

2020

Front. Physiol.

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Tissue inhibitor of metalloproteinase 3 (TIMP3) is unique among the four TIMPs due to its extracellular matrix (ECM)-binding property and broad range of inhibitory substrates that includes matrix metalloproteinases (MMPs), a disintegrin and metalloproteinases (ADAMs), and ADAM with thrombospondin motifs (ADAMTSs). In addition to its metalloproteinase-inhibitory function, TIMP3 can interact with proteins in the extracellular space resulting in its multifarious functions. TIMP3 mRNA has a long 3' untranslated region (UTR) which is a target for numerous microRNAs. TIMP3 levels are reduced in various cardiovascular diseases, and studies have shown that TIMP3 replenishment ameliorates the disease, suggesting a therapeutic potential for TIMP3 in cardiovascular diseases. While significant efforts have been made in identifying the effector targets of TIMP3, the regulatory mechanism for the expression of this multifunctional TIMP has been less explored. Here, we provide an overview of TIMP3 gene structure, transcriptional and post-transcriptional regulators (transcription factors and microRNAs), protein structure and partners, its role in cardiovascular pathology and its application as therapy, while also drawing reference from TIMP3 function in other diseases.

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Section: Micrornas Bind To and Downregulate Timp3mentioning

confidence: 99%

Section: Micrornas Bind To and Downregulate Timp3mentioning

confidence: 99%

Biology of Tissue Inhibitor of Metalloproteinase 3 (TIMP3), and Its Therapeutic Implications in Cardiovascular Pathology

Fan

Kassiri

2020

Front. Physiol.

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“…Cardiovascular disease (CVD) is one of the leading causes of death in the developed countries [1]. Heart failure (HF) is the fastest growing CVD in the world which poses a significant global burden, affecting nearly 26 million people worldwide [2].…”

Section: Introductionmentioning

confidence: 99%

Mapping the Minnesota living with heart failure questionnaire (MLHFQ) to EQ-5D-5L in patients with heart failure

Kularatna

Senanayake

Chen

et al. 2020

Health Qual Life Outcomes

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Background: Mapping algorithms can be used to convert scores from a non-preference based instrument to health state utilities. The objective of this study was to develop mapping algorithms which will enable the Minnesota Living with Heart Failure Questionnaire (MLHFQ) scores to be converted into EQ-5D-5L utility scores that can be used in heart failure related cost utility studies. Method: Patients diagnosed with heart failure were recruited from Australia. Mapping algorithms were developed using both direct and indirect response mapping approach. Three model specifications were considered to predict the EQ-5D-5 L utility score using MLHFQ total score (Model 1), MLHFQ domain scores (Model 2), or MLHFQ item scores (Model 3). Six regression techniques, each of which has the capability to cope with either skewness, heteroscedasticity, ceiling effects and/or the potential presence of outliers in the data set were used to identify the optimal mapping functions for each of the three models. Goodness-of-fit of the models were assessed using six indicators. In the absence of an external validation dataset, predictive performance of was assessed using threefold cross validation method. In the indirect response mapping, EQ. 5D 5 L responses were predicted separately using the MLHFQ item scores using ordered logit model. Results: A total of 141 patients participated in the study. The lowest mean absolute error (MAE) was recorded from the multivariable fractional polynomials (MFP) model in all three-model specifications. Regarding the indirect response mapping, results showed that the performance was comparable with the direct mapping approach based on root mean squared error (RMSE) but was worse based on MAE. Conclusion: The MLHFQ can be mapped onto EQ-5D-5 L utilities with good predictive accuracy using both direct and indirect response mapping techniques. The reported mapping algorithms would facilitate calculation of health utility for economic evaluations related to heart failure.

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“…5,6 The miRNA biogenesis pathway is closely connected with heart functions and is involved in regulating angiogenesis, 7 heart development, 8 heart failure, 9 and ischemia reperfusion-injury (IRI). 5,6 The miRNA biogenesis pathway is closely connected with heart functions and is involved in regulating angiogenesis, 7 heart development, 8 heart failure, 9 and ischemia reperfusion-injury (IRI).…”

Section: Introductionmentioning

confidence: 99%

“…Previous research on MIRI indicates a principal role of microRNAs (miRNAs), the noncoding RNAs that significantly regulate cell differentiation, cycle, proliferation, and apoptosis, and are extensively expressed in different organs and tissues. 5,6 The miRNA biogenesis pathway is closely connected with heart functions and is involved in regulating angiogenesis, 7 heart development, 8 heart failure, 9 and ischemia reperfusion-injury (IRI). 7 miRNA expressions are considerably regulated in the myocardial ischemia process and hypoxia.…”

Section: Introductionmentioning

confidence: 99%

miR‐496 remedies hypoxia reoxygenation–induced H9c2 cardiomyocyte apoptosis via Hook3‐targeted PI3k/Akt/mTOR signaling pathway activation

Jin

Ni²

2019

J of Cellular Biochemistry

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The hypoxia‐reoxygenation (H/R) model helps analyze myocardial infarction triggered by acute myocardial ischemia, which induces cardiomyocyte proliferation and apoptosis. The Gene Expression Omnibus database was used to obtain the GSE74205 and GSE3866 microarray data, including microRNA (miRNA) and messenger RNA profiles, to catalog potential key miRNAs and genes. The role of rno‐mir‐496 expression in cardiomyocyte proliferation within 10 days of birth was established. The microRNA Target Prediction Database (miRDB) database—via Gene Ontology annotation—predicted hook microtubule tethering protein 3 (Hook3), a key target gene of rno‐mir‐496, was closely related to cell proliferation. Upregulation of miR‐496 related to a significant reduction in apoptosis of H9c2 and human cardiomyocytes treatment with H/R. Moreover, transfection of H9c2 cells with miR‐496 mimics, which were pretreated with H/R for 12 hours, increased Ki67 levels, proliferating cell nuclear antigen and Bcl‐2 proteins; and decreased cleaved caspase‐3 and Bax protein levels, as determined by reverse transcription‐polymerase chain reaction and Western blot assays. A dual‐luciferase reporter system confirmed that miR‐496 targets the Hook3 suppressor. Hook3 overexpression stimulated apoptosis in H/R‐treated cells, thus reducing cell proliferation. Upregulated miR‐496 activated phosphatidylinositol‐3‐kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling, while Hook3 exhibited the inverse trend in H/R‐treated H9c2 cells. In summary, with Hook3 functionality's aid, miR‐496 upregulation defends cells from H/R‐induced apoptosis and stimulates cell proliferation. miR‐496 targets Hook3 to trigger the PI3K/Akt/mTOR signaling pathway for antiapoptotic and proliferative effects.

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The relevance of microRNA in post-infarction left ventricular remodelling and heart failure

Cited by 30 publications

References 70 publications

Biology of Tissue Inhibitor of Metalloproteinase 3 (TIMP3), and Its Therapeutic Implications in Cardiovascular Pathology

Biology of Tissue Inhibitor of Metalloproteinase 3 (TIMP3), and Its Therapeutic Implications in Cardiovascular Pathology

Mapping the Minnesota living with heart failure questionnaire (MLHFQ) to EQ-5D-5L in patients with heart failure

miR‐496 remedies hypoxia reoxygenation–induced H9c2 cardiomyocyte apoptosis via Hook3‐targeted PI3k/Akt/mTOR signaling pathway activation

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