B cell translocation gene, a direct target of miR‐142‐5p, inhibits vascular smooth muscle cell proliferation by down‐regulating cell cycle progression

Abstract

a b s t r a c tVascular smooth muscle cell (VSMC) proliferation plays a key role in neointimal hyperplasia and restenosis. Here we report the role of the microRNA miR-142-5p and its downstream target genes on the proliferation of cultured VSMCs. miR-142-5p promoted VSMC proliferation by down-regulating B cell translocation gene 3 (BTG3). We found that BTG3 inhibited the expression of cell cycle regulatory genes and cell growth. As shown by luciferase reporter assay, miR-142-5p bound directly to the 3 0 -untranslated region of BTG3. Overexpression of miR-142-5p induced expression of cell cycle regulatory genes. Thus, BTG3, a novel, direct target of miR-142-5p, negatively regulates VSMC proliferation.

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

“…Barsanti et al [20] found that the expression levels of identified miRNAs, including miR-142-5p, were correlated with offpump cardiac index values and may contribute to the molecular regulation of reverse remodeling and heart recovery mechanisms. Molecular function analyses revealed that the B-cell translocation gene may be a direct target of miR-142-5p, which regulates vascular cell proliferation [25]. We hypothesized significant associations among miR-142, platelet reactivity and the risk of cardiovascular events based on the role of miR-142 in cardiovascular diseases.…”

MicroRNA regulatory pathway analysis identifies miR-142-5p as a negative regulator of TGF-β pathway via targeting SMAD3

“…Recent researches have indicated a controversial function for miR-142-5p in cell growth and cell progression. MiRNA profiling of clinical samples and cell lines has shown that miR-142-5p is upregulated in vascular smooth muscle cells [34], and downregulated in renal cell carcinoma and systemic lupus erythematosus [35–37], indicating that miR-142-5p could suppress cell growth or promotes cell proliferation in different conditions. Our investigations indicated that miR-142-5p is highly and differentially expressed in some tumor cells, indicating that miR-142-5p functions an oncogenic role by suppressing the translation of SMAD3 to promote cancer cell growth.…”

Transcriptomic profiling of platelet senescence and platelet extracellular vesicles

“…Up‐regulated PL‐EV miRs represent circulating miR species that are regulated in type 2 diabetes (miR‐144‐3p, miR‐486‐5p), miR‐142‐5p, coronary artery disease (miR‐451a, miR‐25‐3p), miR‐145‐5p, pre‐eclampsia, MI (let‐7f‐5p), obesity (miR‐486‐5p), and metabolic risk, supporting the potential of these miR species as biomarkers for vascular and metabolic disease screening. Molecular function analyses have revealed that miR‐144‐3p targets ABCA1, which regulates lipid metabolism and plasma high‐density lipoprotein levels; miR‐142‐5p targets B‐cell translocation gene 3, which regulates vascular cell proliferation; miR‐484 targets Fis1, which regulates mitochondria fission/fusion and apoptosis; and let‐7c targets the B‐cell lymphoma 2 (Bcl2) cell death antagonist, which regulates apoptosis . Target sequences also were detected within several mRNAs encoding the proteins that regulate PLT adhesion, activation, and coagulation (Table S3), connecting the known role of PL‐EVs in atherothrombosis …”