Platelet MicroRNA 365-3p Expression Correlates with High On-treatment Platelet Reactivity in Coronary Artery Disease Patients

Chen, Yueh Chung; Lin, Feng Yen; Lin, Yi Wen; Cheng, Soo‐Chen; Chang, Chao; Lin, Rong; Chuang, Chun Ling; Sheu, Jehn Shing; Chen, Shan Min; Tsai, Chien‐Sung

doi:10.1007/s10557-019-06855-3

Cited by 19 publications

(34 citation statements)

References 34 publications

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“…32,53,54 Similarly, several other platelet miRs were reported to correlate with ontreatment platelet reactivity, including miR-126, miR-92a, miR-26a, and miR-365-3p. 32,[55][56][57] MiR-126 and miR-223 showed strong correlation with platelet function tests in plasma of patients on dual antiplatelet therapy 1 month after ACS. 32 Furthermore, inhibition of miR-126 leads to reduced platelet aggregation and receptor expression in mice.…”

Section: Platelets Micrornas In Antiplatelet Drug Resistancementioning

confidence: 92%

MicroRNAs as Regulators and Biomarkers of Platelet Function and Activity in Coronary Artery Disease

et al. 2019

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Microribonucleic acids (miRs) are small, noncoding ribonucleic acids (RNAs), which play an important role in the regulation of platelet function and activity. Several studies proposed a mechanistic role of platelet-related miRs in the pathophysiology of coronary artery disease (CAD) and atherothrombosis. Circulating, platelet-related miRs have been proposed as diagnostic, prognostic, as well as treatment response biomarkers in CAD and acute coronary syndrome (ACS). In this review, we summarize recent studies on the role of platelet-related miRs in the regulation of platelet function and activity. Furthermore, we review the studies investigating the role of platelet-related miRs as biomarkers in patients with CAD and ACS.

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Section: Platelets Micrornas In Antiplatelet Drug Resistancementioning

confidence: 92%

MicroRNAs as Regulators and Biomarkers of Platelet Function and Activity in Coronary Artery Disease

et al. 2019

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“…46 Of note, the expression of miR-365a-3p was sustained at a high level in patients with abnormal and overactive platelet. 47 Upregulated miR-365a-3p was also observed in intracerebral hemorrhage patients, 48 and further supports a role for miR-365a-3p in hemostatic pathways. Consistent miR-365a-3p-driven suppression on tissue factor expression and function indicates that miR-365a-3p has a new fine-tuning role in modulating the tissue factor regulatory pathway.…”

Section: Discussionmentioning

confidence: 61%

Estradiol-Responsive miR-365a-3p Interacts with Tissue Factor 3′UTR to Modulate Tissue Factor-Initiated Thrombin Generation

et al. 2021

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Background: High oestradiol (E2) levels are linked to an increased risk of venous thromboembolism, however, the underlying molecular mechanism(s) remain poorly understood. We previously identified an E2-responsive microRNA (miR), miR-494-3p that downregulates protein S expression, and posited additional coagulation factors, such as tissue factor, may be regulated in a similar manner via miRs. Objectives: To evaluate the coagulation capacity of cohorts with high physiological E2, and to further characterise novel E2-responsive miR and miR regulation on tissue factor in E2-related hypercoagulability. Methods: Ceveron® Alpha thrombin generation assay (TGA) was used to assess plasma coagulation profile of three cohorts. The effect of physiological levels of E2, 10 nM on miR expression in HuH-7 cells was compared using NanoString nCounter® and validated with independent assays. The effect of tissue factor interacting miR was confirmed by dual-luciferase reporter assays, immunoblotting, flow cytometry, biochemistry assays and TGA. Results: Plasma samples from pregnant women and women on the contraceptive pill were confirmed to be hypercoagulable (compared with sex-matched controls). At equivalent and high physiological levels of E2, miR-365a-3p displayed concordant E2-down-regulation in two independent miR quantification platforms, and tissue factor mRNA (F3) was up-regulated by E2 treatment. Direct interaction between miR-365a-3p and F3-3’UTR was confirmed and overexpression of miR-365a-3p led to a decrease of 1) tissue factor mRNA transcripts, 2) protein levels, 3) activity and 4) tissue factor-initiated thrombin generation. Conclusion: miR-365a-3p is a novel tissue factor regulator. High E2 concentrations induces a hypercoagulable state via a miR-network specific for coagulation factors.

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“…Another study also showed that inhibition of platelet reactivity in healthy volunteers with prasugrel or DAPT containing prasugrel decreased the circulating miR-223-3p (62). In patients with coronary artery disease who received antiplatelet treatment for 24 h, the severity of coronary artery disease based on SYNTAX score was positively correlated with the platelet level of miR-223-3p, which might indirectly reflect the relation between platelet reactivity and miR-223-3p (110). Thus, although miR-223-3p can inhibit P2Y12 in platelets to affect the platelet reactivity, the circulating miR-223-3p levels may also be influenced by degree of P2Y12 inhibition and associated with platelet reactivity, and as a result, the definite correlation between circulating miR-223-3p levels and platelet reactivity might depend on status of patients, categories of drugs, or administration time.…”

Section: Role Of Mir-223-3p In Antiplatelet Therapymentioning

confidence: 94%

MiR-223-3p in Cardiovascular Diseases: A Biomarker and Potential Therapeutic Target

Zhang

Shen

Shi

et al. 2021

Front. Cardiovasc. Med.

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Cardiovascular diseases, involving vasculopathy, cardiac dysfunction, or circulatory disturbance, have become the major cause of death globally and brought heavy social burdens. The complexity and diversity of the pathogenic factors add difficulties to diagnosis and treatment, as well as lead to poor prognosis of these diseases. MicroRNAs are short non-coding RNAs to modulate gene expression through directly binding to the 3′-untranslated regions of mRNAs of target genes and thereby to downregulate the protein levels post-transcriptionally. The multiple regulatory effects of microRNAs have been investigated extensively in cardiovascular diseases. MiR-223-3p, expressed in multiple cells such as macrophages, platelets, hepatocytes, and cardiomyocytes to modulate their cellular activities through targeting a variety of genes, is involved in the pathological progression of many cardiovascular diseases. It participates in regulation of several crucial signaling pathways such as phosphatidylinositol 3-kinase/protein kinase B, insulin-like growth factor 1, nuclear factor kappa B, mitogen-activated protein kinase, NOD-like receptor family pyrin domain containing 3 inflammasome, and ribosomal protein S6 kinase B1/hypoxia inducible factor 1 α pathways to affect cell proliferation, migration, apoptosis, hypertrophy, and polarization, as well as electrophysiology, resulting in dysfunction of cardiovascular system. Here, in this review, we will discuss the role of miR-223-3p in cardiovascular diseases, involving its verified targets, influenced signaling pathways, and regulation of cell function. In addition, the potential of miR-223-3p as therapeutic target and biomarker for diagnosis and prediction of cardiovascular diseases will be further discussed, providing clues for clinicians.

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Platelet MicroRNA 365-3p Expression Correlates with High On-treatment Platelet Reactivity in Coronary Artery Disease Patients

Cited by 19 publications

References 34 publications

MicroRNAs as Regulators and Biomarkers of Platelet Function and Activity in Coronary Artery Disease

MicroRNAs as Regulators and Biomarkers of Platelet Function and Activity in Coronary Artery Disease

Estradiol-Responsive miR-365a-3p Interacts with Tissue Factor 3′UTR to Modulate Tissue Factor-Initiated Thrombin Generation

MiR-223-3p in Cardiovascular Diseases: A Biomarker and Potential Therapeutic Target

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