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34 results for “MiR-126”
miR-126 promotes M1 to M2 macrophage phenotype switching via VEGFA and KLF4
<p><strong>Background. </strong>Macrophage polarization and microRNA play crucial roles in the development of atherosclerosis (AS). The M1 macrophage phenotype contributes to the formation of plaques, while the M2 macrophage phenotype resolves inflammation and promotes tissue repair. MiR-126 has been found to play a role in regulating macrophage polarization in the context of AS. However, the exact mechanism of miR-126 requires further research.</p> <p><strong>Methods.</strong> The foam cell model was established by stimulating THP-1 with oxidized low-density lipoprotein (ox-LDL). We transfected foam cells with miR-126 mimic and its negative control. The transfection of miR-126 was implemented by riboFECT CP transfection kit. The levels of miR-126 and M1/M2 associated genes in foam cells were quantified using reverse transcription-quantitative PCR (RT-qPCR). Additionally, the expressions of CD86<sup>+</sup> and CD206<sup>+</sup> cells in foam cells were determined by flow cytometry. Western blotting and RT-qPCR were used to determine the protein and mRNA levels of the vascular endothelial growth factor A (VEGFA) and the transcriptional regulator Krüppel-like factor 4 (KLF4), respectively. Additionally, we detected endothelial cell migration after co-culturing endothelial cells and macrophages. MG-132 was used to indirectly activate the expression of VEGFA, and the expression of KLF4 was also evaluated.</p> <p><strong>Results. </strong>The activation of apoptosis and production of foam cells were boosted by the addition of ox-LDL. We transfected foam cells with miR-126 mimic and its negative control and observed that miR-126 greatly suppressed foam cell development and inhibited phagocytosis. Moreover, it caused pro-inflammatory M1 macrophages to switch to the anti-inflammatory M2 phenotype. This was reflected by the increase in anti-inflammatory gene expression and the decrease in pro-inflammatory gene expression. Additionally, miR-126 dramatically decreased the expressions of VEGFA and KLF4. The protein-protein interaction network analysis showed a significantly high correlation between miR-126, VEGFA, and KLF4. MiR-126 may also promote EC migration by activating macrophage PPAR γ expression and effectively suppressing macrophage inflammation. MG-132 indirectly activated the expression of VEGFA, and the expression of KLF4 also significantly increased, which indicates a direct or indirect relationship between VEGFA and KLF4.</p> <p><strong>Conclusion.</strong> Our study shows that miR-126 can reverse ox-LDL-mediated phagocytosis and apoptosis in macrophages. Consequently, the potential role of miR-126 was manifested in regulating macrophage function and promoting vascular endothelial migration.</p>
Data from: GATA2 controls lymphatic endothelial cell junctional integrity and lymphovenous valve morphogenesis through miR-126
Mutations in the transcription factor GATA2 cause lymphedema. GATA2 is necessary for the development of lymphatic valves (LVs) and lymphovenous valves (LVVs), and for the patterning of lymphatic vessels. Here, we report that GATA2 is not necessary for valvular endothelial cell (VEC) differentiation. Instead, GATA2 is required for VEC maintenance and morphogenesis. GATA2 is also necessary for the expression of cell junction molecules VE-Cadherin and Claudin5 in lymphatic vessels. We identified miR-126 as a target of GATA2, and miR-126-/- embryos recapitulate the phenotypes of mice lacking GATA2. Primary human lymphatic endothelial cells (HLECs) lacking GATA2 (GATA2ΔHLEC) have altered expression of Claudin5 and VE-Cadherin, and blocking miR-126 activity in HLECs phenocopies these changes in expression. Importantly, overexpression of miR-126 in GATA2ΔHLEC significantly rescues the cell junction defects. Thus, our work defines a new mechanism of GATA2 and uncovers miR-126 as a novel regulator of mammalian lymphatic vascular development.
Data from: GATA2 controls lymphatic endothelial cell junctional integrity and lymphovenous valve morphogenesis through miR-126
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Raw data for the article: MicroRNA-30d and -483-3p for bi-ventricular remodelling and miR-126-3p for pulmonary hypertension in advanced heart failure
<p><strong>Aims: </strong>MicroRNAs play a role in pathogenic mechanisms leading to heart failure. We measured a panel of 754 miRNAs in the myocardial tissue and in the serum of patients with heart failure with reduced ejection fraction due to dilatative idiopathic cardiomyopathy (DCM, N = 10) or ischaemic cardiomyopathy (N = 3), referred to left ventricular assist device implant. We aim to identify circulating miRNAs with high tissue co-expression, significantly associated to echocardiographic and haemodynamic measures.</p> <p><strong>Methods and results: </strong>We have measured a panel of 754 miRNAs in the myocardial tissue [left ventricular (LV) apex] and in the serum obtained at the same time in a well selected study population of end-stage heart failure with reduced ejection fraction due to either DCM or ischaemic cardiomyopathy, referred to continuous flow left ventricular assist device implant. We observed moderate agreement for miR-30d, miR-126-3p, and miR-483-3p. MiR-30d was correlated to LV systolic as well as diastolic volumes (r = 0.78, P = 0.001 and r = 0.80, P = 0.005, respectively), while miR-126-3p was associated to mPAP and PCWP (r = -0.79, P = 0.007 and r = -0.80, P = 0.005, respectively). Finally, serum miR-483-3p had an association with right ventricular end diastolic diameter (r = -0.73, P = 0.02) and central venous pressure (CVP) (r - 0.68 p 0.03).</p> <p><strong>Conclusions: </strong>In patients with DCM, few miRNAs are co-expressed in serum and tissue: They are related to LV remodelling (miR-30d), post-capillary pulmonary artery pressure (miR-126-3p), and right ventricular remodelling/filling pressures (miR-483-3p). Further studies are needed to confirm their role in diagnosis, prognosis or as therapeutic targets in heart failure with reduced ejection fraction.</p>
Gene Expression Profile for the identification of miR-126 targets
GEO Series GSE32089. Homo sapiens. 8 samples. Type: Expression profiling by array.
Genomewide expression profile of wire-injured carotid arteries harvested from either miR-126+/+/ApoE-/- or miR-126-/-/ApoE-/- mice during neointima development
GEO Series GSE34262. Mus musculus. 8 samples. Type: Expression profiling by array.
miR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease [BulkRNA 1]
GEO Series GSE236138. Homo sapiens. 16 samples. Type: Expression profiling by high throughput sequencing.
miR-126 Governs Human Leukemia Stem Cell Quiescence and Therapeutic Resistance [miRNA]
GEO Series GSE55916. Homo sapiens. 123 samples. Type: Non-coding RNA profiling by array.
Muscle Exosome-Derived miR-126 Regulates Local Synthesis of TDP-43 and NMJ Integrity in ALS
GEO Series GSE286913. Mus musculus. 18 samples. Type: Non-coding RNA profiling by high throughput sequencing; Expression profiling by high throughput sequencing.
miR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease [RNASeq 2]
GEO Series GSE236141. Homo sapiens. 14 samples. Type: Expression profiling by high throughput sequencing.
Attenuation of miR-126 activity expands HSC in vivo without exhaustion
GEO Series GSE40458. Homo sapiens. 12 samples. Type: Expression profiling by array.
miR-126-5p by direct targeting of JNK-interacting protein-2 (JIP-2) plays a key role in Theileria-infected macrophage virulence
GEO Series GSE97706. Bos taurus. 17 samples. Type: Non-coding RNA profiling by high throughput sequencing.
Targeting miR-126 in inv(16) acute myeloid leukemia inhibits leukemia development and leukemia stem cell maintenance
GEO Series GSE184015. Mus musculus. 10 samples. Type: Expression profiling by high throughput sequencing.
miR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease [scRNAseq]
GEO Series GSE236136. Homo sapiens. 5 samples. Type: Expression profiling by high throughput sequencing.
Association of Elevated Urinary miR-126, miR-155 and miR-29b with Diabetic Kidney Disease
GEO Series GSE114477. Homo sapiens. 8 samples. Type: Expression profiling by RT-PCR.
miR-126-3p contributes to parathyroid tumor angiogenesis
<p>Tumors of the parathyroid glands are highly vascularized and display a microRNA (miRNA) profile divergent from normal parathyroid glands (PaNs). Angiogenic miRNAs, namely miR-126-3p, miR-126-5p, and miR-296-5p, have been found downregulated in parathyroid tumors. Here, we show that miR-126-3p expression levels are reduced in parathyroid adenomas (PAds; n = 12) compared with PaNs (n = 4). In situ hybridization (ISH) of miR-126-3p and miR-296-5p in 10 PAds show that miR-126-3p is expressed by endothelial cells lining the walls of great vessels and by cells within the thin stroma surrounding acinar structures. At variance, miR-296-5p was detectable in most PAd epithelial cells. Combining ISH for miR-126-3p with immunohistochemistry for the endothelial and mesenchymal markers CD34, CD31 and α-smooth muscle actin (αSMA), we could identify that miR-126-3p is localized in the αSMA-positive thin stroma. Further, miR-126-3p-expressing cells are enriched in the CD34-positive stromal cells surrounding epithelial cell acinar structures, a cellular pattern consistent with tumor-associated myofibroblasts (TAMs). In line with this, CD34-positive cells, sorted by FACS from PAds tissues, express miR-126-3p at higher levels than CD34-negative cells, suggesting that miR-126-3p downregulation promotes the endothelial-to-αSMA+ mesenchymal transition. In human mesenchymal stem cells derived from bone marrow (hBM-MSCs), a model of TAMs, the co-culture with PAds-derived cells for 5 days decreases miR-126-3p, while it increases VEGFA expression. At variance, adrenomedullin (ADM) expression is unaffected. Finally, overexpression of the miR-126-3p mimic in both hBM-MSCs and PAds-derived explants downregulates VEGFA expression levels. In conclusion, miR-126-3p is expressed by both endothelial cells and TAMs in PAds, and its downregulation promotes neoangiogenesis, possibly through VEGFA overexpression.</p>
Circulating miR-126 as a Novel Biomarker for Post Myocardial Infarction Remodeling
ClinicalTrials.gov study NCT01875484. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Effect of Exercise on MiR-126 in Individuals With Prediabetes
ClinicalTrials.gov study NCT06809257. IPD Sharing: NO. Countries: 1. Publications: 0.
miR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease
GEO Series GSE236142. Homo sapiens. 35 samples. Type: Expression profiling by high throughput sequencing.
miR-126 governs human leukemia stem cell quiescence and therapeutic resistance
GEO Series GSE55770. Homo sapiens. 74 samples. Type: Other.
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Allen Brain Atlas
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DANDI Archive for NWB datasets
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International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.