1,723,560 research outputs found
miR-30b-5p inhibits osteoblast differentiation through targeting BCL6
No full textHuman bone marrow mesenchymal stem cells (hBMSCs) are attractive candidates for new therapies to improve bone regeneration and repair. This study was to identify the function of the miR-30b-5p/BCL6 axis in osteogenic differentiation of hBMSCs. Realtime-quantitative PCR (RT-qPCR) and Western blotting were used to measure the relative expression of ALP, OCN, RUNX2, miR-30b-5p, and BCL6 during osteogenic differentiation of hBMSCs. The relationship between miR-30b-5p and BCL6 in hBMSCs was identified using dual-luciferase reporter system and RNA pull-down assay. Alizarin red S staining (ARS) was used to detect the calcium nodules in hBMSCs. We found that the expression of miR-30b-5p was downregulated, whereas that of BCL6 was upregulated during osteogenic differentiation of hBMSCs. Downregulating miR-30b-5p enhanced the expression of OCN, RUNX2, and ALP, and promoted calcium deposition. Conversely, transfection with si-BCL6 had the opposite effect that it inhibited osteogenic differentiation. However, the inhibitory effect of si-BCL6 was abrogated by miR-30b-5p inhibitor. miR-30b-5p inhibits the osteogenic differentiation of hBMSCs by targeting BCL6.</p
ROC curves for miR-30b-5p.
No full textDiscrimination capacity between group A and group B1 (A), group A and group B17 (D). MiR-30b-5p can discriminate between healthy and asymptomatic MMVD-affected dogs (stage B1).</p
Marginal effect of plasma miR-30b-5p expression on echocardiographic variables at T0 and T1.
No full textBlack line: T0. Red line: T1. A) Marginal effect of miR-30b-5p on LVIDdN. B) Marginal effect of miR-30b-5p on ESVI: The interaction between the two parameters is high since T0 and T1 lines are poorly parallel. C) Marginal effect of miR-30b-5p on EDVI. D) Marginal effect of miR-30b-5p on LA/Ao.</p
Marginal effect of plasma miR-30b-5p expression on ordinal variables at T0 and T1.
No full textBlack line: T0. Red line: T1. On the y-axis, the probability of the class with the lower value is reported. A) Marginal effect of miR-30b-5p on the presence/intensity of a heart murmur. B) Marginal effect of miR-30b-5p on the mitral regurgitant jet size. C) Marginal effect of miR-30b-5p on the MINE score.</p
The AUC (95% confidence interval), cut off values, and sensitivity and specificity of miR-30b-5p in CKCSs’ plasma.
No full textThe AUC (95% confidence interval), cut off values, and sensitivity and specificity of miR-30b-5p in CKCSs’ plasma.</p
DataSheet_1_Extracellular vesicle-associated microRNA-30b-5p activates macrophages through the SIRT1/ NF-κB pathway in cell senescence.pdf
No full textChronic inflammation is widely observed in aging, but it is unclear whether extracellular vesicles (EVs) play a role in chronic disease-associated senescence. In our study, LC/MS profiling revealed that senescent cell derived EVs (SEN EVs) activate the immune response pathways of macrophages. Significantly more EVs were found in the supernatant of SEN than of control (CON) cell cultures, and SEN EVs were enriched in miR-30b-5p, which directly target sirtuin1 (SIRT1). In vitro, we found that SEN EV treatment resulted in increased cellular levels of interleukin-1β (IL-1β) and IL-6 and decreased levels of SIRT1. Increased cytokine levels could be reversed by SIRT1 activation and miR-30b-5p inhibition. Furthermore, miR-30b-5p significantly increased with age in both mouse liver tissue and EVs harvested from the tissue, with differences in EVs observed both earlier and in the later magnitude of aging. Western blot and qPCR proved that miR-30b-5p downregulated the level of SIRT1 in mouse macrophages. Collectively, we propose that EVs carrying miR-30b-5p from SEN cells can induce chronic inflammation through macrophage activation. This occurs through the downregulation of SIRT1 and the corresponding activation of NF-κB pathways that enhance pro-inflammatory cytokine production. Collectively, these results demonstrate that EVs carrying pro-inflammatory signals are released by SEN cells and then activate immune cells in the SEN microenvironment, changing the inflammatory balance. Our results also explain why inflammation increases with age even though SEN cells can be immediately eliminated under rigorous immune surveillance.</p
Expression levels of miR-1-3p, miR-30b-5p, and miR-128-3p between groups.
No full textExpression levels of the three miRNAs between groups A and B1 (A-C, respectively) and between A and B1 were divided according to the age at MMVD diagnosis (D-F, respectively). MiR-30b-5p increased 2.4 folds (P P = 0.034), B1 3–7 (2.2 folds, P = 0.028), and B1>7 (2.7 folds, P = 0.018) expressed a higher level of miR-30b-5p than group A. No differences were found in the amount of miR-1-3p (A and D) and miR-128-3p (C and F).</p
Additional file 11 of miR-30b-5p inhibits proliferation, invasion, and migration of papillary thyroid cancer by targeting GALNT7 via the EGFR/PI3K/AKT pathway
No full textAdditional file 11. Differential expression of miR-30b-5p in patients with braf mutant and wild type thyroid carcinoma
Data_Sheet_1_Downregulation of Neurofilament Light Chain Expression in Human Neuronal-Glial Cell Co-Cultures by a Microbiome-Derived Lipopolysaccharide-Induced miRNA-30b-5p.pdf
No full textMicrobiome-derived Gram-negative bacterial lipopolysaccharide (LPS) has been shown by multiple laboratories to reside within Alzheimer's disease (AD)-affected neocortical and hippocampal neurons. LPS and other pro-inflammatory stressors strongly induce a defined set of NF-kB (p50/p65)-sensitive human microRNAs, including a brain-enriched Homo sapien microRNA-30b-5p (hsa-miRNA-30b-5p; miRNA-30b). Here we provide evidence that this neuropathology-associated miRNA, known to be upregulated in AD brain and LPS-stressed human neuronal-glial (HNG) cells in primary culture targets the neurofilament light (NF-L) chain mRNA 3'-untranslated region (3'-UTR), which is conducive to the post-transcriptional downregulation of NF-L expression observed within both AD and LPS-treated HNG cells. A deficiency of NF-L is associated with consequent atrophy of the neuronal cytoskeleton and the disruption of synaptic organization. Interestingly, miRNA-30b has previously been shown to be highly expressed in amyloid-beta (Aβ) peptide-treated animal and cell models, and Aβ peptides promote LPS entry into neurons. Increased miRNA-30b expression induces neuronal injury, neuron loss, neuronal inflammation, impairment of synaptic transmission, and synaptic failure in neurodegenerative disease and transgenic murine models. This gut microbiota-derived LPS-NF-kB-miRNA-30b-NF-L pathological signaling network: (i) underscores a positive pathological link between the LPS of gastrointestinal (GI)-tract microbes and the inflammatory neuropathology, disordered cytoskeleton, and disrupted synaptic signaling of the AD brain and stressed brain cells; and (ii) is the first example of a microbiome-derived neurotoxic glycolipid having significant detrimental miRNA-30b-mediated actions on the expression of NF-L, an abundant neuron-specific filament protein known to be important in the maintenance of neuronal cell shape, axonal caliber, and synaptic homeostasis.</p
Image_5_MiR-27a-3p and miR-30b-5p inhibited-vitamin D receptor involved in the progression of tuberculosis.TIFF
No full textBackgroundMicroRNAs (miRNAs) play a vital role in tuberculosis (TB). Vitamin D receptor (VDR), an miRNA target gene, and its ligand, vitamin D3 (VitD3), have been reported to exert protective effects against TB. However, whether miRNAs can affect the progression of TB by targeting VDR has not been reported.Materials and methodsResearch subjects were selected according to defined inclusion criteria. A clinical database of 360 samples was established, including the subjects’ demographic information, miRNA expression profiles and cellular experimental results. Two candidate miRNAs, miR-27a-3p, and miR-30b-5p, were identified by a high-throughput sequencing screen and validated by qRT–PCR assays. Univariate and multivariate statistical analyses were performed. VDR and NF-kB p65 protein levels were detected by Western blot assays. Proinflammatory cytokine expression levels were detected by enzyme-linked immunosorbent assay (ELISA). Luciferase assays and fluorescence-activated cell sorting (FACS) were further applied to elucidate the detailed mechanisms.ResultsDifferential miRNA expression profiles were obtained, and miR-27a-3p and miR-30b-5p were highly expressed in patients with TB. These results showed that the two miRNAs were able to induce M1 macrophage differentiation and inhibit M2 macrophage differentiation. Further experiments showed that the two miRNAs decreased the VDR protein level and increased proinflammatory cytokine secretion by macrophages. Mechanistically, the miRNAs targeted the 3′ untranslated region (3′UTR) of the VDR mRNA and thereby downregulated VDR protein levels by post-transcriptional regulation. Then, due to the reduction in VDR protein levels, the NF-kB inflammatory cytokine signaling pathway was activated, thus promoting the progression of TB.ConclusionOur study not only identified differentially expressed miRNAs between the TB and control groups but also revealed that miR-27a-3p and miR-30b-5p regulate proinflammatory cytokine secretion and macrophage differentiation through VDR in macrophages. Thus, these two miRNAs influence the progression of TB.</p
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