Our results show miR-150 (p<0.01) and to a lesser extent miR-146b-5p (p<0.05) levels in PBMCs to reliably distinguish between ART-naïve AIDS patients, those on ART, and those developing drug resistance and failing ART.
We aimed to explore whether microRNA-150 (miR-150) regulates endothelial cell function and vascular remodeling in acute coronary syndrome (ACS), and the involvement of PTX3 and NF-κB signaling pathway.
These findings also suggest that manipulating the levels of miRNA-150 could be a valuable strategy in prevention and/or treatment of acute graft-versus-host disease.
Microarray analysis identified miRNAs highly expressed in the serum of patients with AIP: 13 miRNAs vs. CP, 204 miRNAs vs. pancreatic cancer, and 19 miRNAs vs. healthy controls. miR-150-5p was commonly upregulated in AIP compared to the other samples.
Microarray analysis identified miRNAs highly expressed in the serum of patients with AIP: 13 miRNAs vs. CP, 204 miRNAs vs. pancreatic cancer, and 19 miRNAs vs. healthy controls. miR-150-5p was commonly upregulated in AIP compared to the other samples.
In this study, we found that miR-150 is downregulated in samples from patients with acute lymphoblastic leukemia, acute myeloid leukemia, and chronic myeloid leukemia, and normalized after patients achieved complete remission.
Of note, analysis of human acute lymphoblastic leukemia (ALL) cohorts also revealed an inverse relationship between miR-150-5p expression and disease progression.
Significant overexpression of hsa-miR-451a, hsa-miR-486-5p, hsa-miR-363-3p, and hsa-miR-150-5p was confirmed in AML relative to ACA and ACC. hsa-miR-184, hsa-miR-483-5p, and hsa-miR-183-5p were significantly overexpressed in ACC relative to ACA but not to AML.
We found that plasma levels of miR-22-5p and miR-150-3p were significantly higher during the early stage of AMI and their expression levels peaked earlier than cTnI.
Low circulating levels of miR-150 are associated with LV remodeling after first ST-segment-elevation acute myocardial infarction. miR-150 has potential as a novel biomarker in this setting.
In vivo studies showed that overexpression of miR-150 in mice resulted in improved cardiac function, reduced myocardial infarction size, inhibition of apoptosis, and reduced inflammatory Ly-6C(high) monocyte invasion levels after AMI.
By overexpressing or knocking down miR-150 in lung adenocarcinoma A549 cells and H1975 cells, it was experimentally validated that miR-150 is a direct regulator of SRCIN1.
There was a very strong difference in the expression level of miR-150 between lung adenocarcinoma patients and lung squamous cell carcinoma patients (P < 0.0001).
Interactions involving SNHG16-miR-146a-5p-SMAD4 and RP6-24A23.7-miR-342-3p/miR-150-5p-EP300 were highlighted according to the lncRNA-miRNA-mRNA network. miR-146a-5p, miR-342-3p, and miR-150-5p are lymphatic metastasis-related miRNAs in lung adenocarcinoma.
A total of 41 and 26 genes were identified as <i>miR-150-5p</i> and <i>miR-150-3p</i> targets, respectively, and they were closely involved in LUAD pathogenesis.
miRNA-150 and miRNA-375 expression was significantly decreased in AdCC and PAC compared with salivary gland tissue controls, whilst miRNA-455-3p showed significantly increased expression in AdCC when compared to PAC, (P < 0.05). miR-150, miR-357 and miR-455-3p expression in AdCC, PAC and control was not associated with age, gender nor with anatomic site (major and minor salivary glands) (P > 0.05).