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Tagging Functional Polymorphism in 3' Untranslated Region of Methylene Tetrahydrofolate Reductase and Risk of Ischemic Stroke.

The association between genetic polymorphisms in the exon or untranslated region of the methylenetetrahydrofolate reductase gene (MTHFR) and the risk of human ischemic stroke (IS) has been well-documented. In this study, we focused on a polymorphism previously screened by high-throughput analysis and on its potential function in patients with IS Methods: This hospital-based case-control study was conducted in 400 patients and 400 healthy volunteers. Genotyping was conducted using TaqMan probes. Potential interactions were predicted by multiple bioinformatics analysis. Relative expression levels of MTHFR were detected confirmed by dual-luciferase assay.

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LncRNA Expression Profile of Human Thoracic Aortic Dissection by High-Throughput Sequencing.

In this study, the long non-coding RNA (lncRNA) expression profile in human thoracic aortic dissection (TAD), a highly lethal cardiovascular disease, was investigated.

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Characterization and Analysis of Whole Transcriptome of Giant Panda Spleens: Implying Critical Roles of Long Non-Coding RNAs in Immunity.

Giant pandas, an endangered species, are a powerful symbol of species conservation. Giant pandas may suffer from a variety of diseases. Owing to their highly specialized diet of bamboo, giant pandas are thought to have a relatively weak ability to resist diseases. The spleen is the largest organ in the lymphatic system. However, there is little known about giant panda spleen at a molecular level. Thus, clarifying the regulatory mechanisms of spleen could help us further understand the immune system of the giant panda as well as its conservation.

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Long non-coding RNA NEAT1 plays an important role in sepsis-induced acute kidney injury by targeting miR-204 and modulating the NF-κB pathway.

This study aimed to explore the role of long non-coding RNA NEAT1 in sepsis-induced acute kidney injury (AKI). The expression levels of NEAT1 in sepsis-induced AKI patients were detected. The rat mesangial cells (RMCs) were treated with lipopolysaccharide (LPS) to induce cell injury. Then, the effects of NEAT1 suppression on the cell viability, apoptosis, cytokines expression, and oxidative stress in the LPS-stimulated RMCs were tested. The regulatory miRNA of NEAT1, as well as the target genes of this miRNA, were investigated. Moreover, the regulatory relationship between NEAT1 and the NF-κB pathway was explored. The results demonstrated that NEAT1 was significantly upregulated in the sepsis-induced AKI patients. Moreover, the upregulation of NEAT1 was associated with the serious degrees of AKI in sepsis patients. In addition, the suppression of NEAT1 alleviated LPS-induced injury in RMCs. MiR-204 was negatively regulated by NEAT1. Suppression of NEAT1 alleviated LPS-induced injury by overexpression of miR-204. Moreover, IL-6R was a target of miR-204, and the effects of the suppression of NEAT1 on LPS-induced cell injury were caused by inactivating the NF-κB pathway. In conclusion, upregulation of NEAT1 may aggravate the LPS-induced injury by targeting miR-204 and activating the NF-κB pathway. NEAT1 may serve as an important diagnostic marker and therapeutic target in sepsis-induced AKI.

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Eukaryotic translation initiation factor 4AII contributes to microRNA-122 regulation of hepatitis C virus replication.

Hepatitis C virus (HCV) is a positive sense RNA virus that persistently infects human liver, leading to cirrhosis and hepatocellular carcinoma. HCV replication requires the liver-specific microRNA-122 (miR-122). In contrast to canonical miRNA-mediated repression via 3'UTR sites, miR-122 positively regulates HCV replication by a direct interaction with the 5' untranslated region (UTR) of the viral RNA. The protein factor requirements for this unusual miRNA regulation remain poorly understood. Here, we identify eIF4AII, previously implicated in miRNA-mediated repression via 3'UTR sites, as a host factor that is important for HCV replication. We demonstrate that eIF4AII interacts with HCV RNA and that this interaction is miR-122-dependent. We show that effective miR-122 binding to, and regulation of, HCV RNA are reduced following eIF4AII depletion. We find that the previously identified HCV co-factor CNOT1, which has also been implicated in miRNA-mediated repression via 3'UTR sites, contributes to regulation of HCV by eIF4AII. Finally, we show that eIF4AI knockdown alleviates the inhibition of HCV replication mediated by depletion of either eIF4AII or CNOT1. Our results suggest a competition effect between the eIF4A proteins to influence HCV replication by modulation of miR-122 function.

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Circulating and Fecal microRNAs as Biomarkers for Inflammatory Bowel Diseases.

Assessment of the disease activity in inflammatory bowel disease (IBD) is essential for adequate treatment management and reliable noninvasive biomarkers for verification of mucosal healing are still needed. MicroRNAs (miRNAs) are differentially expressed in IBD and cancer. We aimed to evaluate the potential of circulating and fecal miRNAs as diagnostic biomarkers for IBD.

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KCNQ1OT1 promotes melanoma growth and metastasis.

Melanoma is the deadliest cutaneous neoplasm. To prevent metastasis, early diagnosis and surgical treatment is vital. Long non-coding RNAs (lncRNAs) may serve as biomarkers and therapeutic targets in tumors. We investigated the molecular mechanisms of lncRNA KCNQ1OT1 in melanoma. Real time PCR demonstrated that KCNQ1OT1 expression is up-regulated in melanoma tissues and cells. KCNQ1OT1 promoted cell proliferation and metastasis in melanoma. By directly bindin to miR-153, KCNQ1OT1 acted as a competing endogenous RNA (ceRNA) to de-repress MET expression. Our results may provide the basis for a novel strategy for early detection and/or treatment of melanoma.

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MiR-193a-3p and miR-224 mediate renal cell carcinoma progression by targeting alpha-2,3-Sialyltransferase IV and the phosphatidylinositol 3 kinase/Akt pathway.

Tumor metastasis is a major cause of cancer-related death in renal cell carcinoma (RCC). MicroRNAs (miRNAs) have been widely known to modulate proliferation invasion, metastasis and apoptosis of cancer cells. In this study, we aimed to investigate the function and novel target of miR-193a-3p and miR-224 in RCC. The levels of miR-193a-3p and miR-224 were significantly increased in RCC tissues and RCC cell lines. Alpha-2, 3-Sialyltransferase IV (ST3GalIV) was highly expressed in adjacent nontumor tissues and human normal proximal tubular cell line HK-2 compared to RCC tissues and cell lines. ST3GalIV expression was negatively correlated with miR-193a-3p and miR-224. Further analysis indicated that miR-193a-3p and miR-224 directly targeted ST3GalIV. MiR-193a-3p and miR-224 increased cell proliferation and migration by directly inhibiting ST3GalIV, and this effect was reversed by co-transfection with ST3GalIV in vitro. Overexpression of miR-193a-3p and miR-224 increased RCC cell proliferation in vivo. Furthermore, the phosphatidylinositol 3 kinase (PI3K)/Akt pathway was mediated by miR-193a-3p and miR-224 in RCC cell lines. Collectively, these results suggested that miR-193a-3p and miR-224 played an important role in regulation of RCC by targeting ST3GalIV via PI3K/Akt pathway. This article is protected by copyright. All rights reserved.

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Identification and characterisation of microRNAs and Piwi-interacting RNAs in cockerels' spermatozoa by Solexa sequencing.

1. There has been substantial research focused on the roles of microRNAs (miRNA) and PIWI-interacting RNAs (piRNA) delivered from mammalian spermatozoa, however comparatively little is known about the role of spermatozoa-delivered miRNAs and piRNAs within breeding cockerels' spermatozoa. 2. A small RNA library of cockerels' spermatozoa was constructed using Illumina high-throughput sequencing technology. Unique sequences with lengths of 18-26 nucleotides were mapped to miRBase 21.0 and unique sequences with lengths of 25-37 nucleotides were mapped to a piRNA database. A total of 1,311 miRNAs and 2,448 potential piRNAs were identified. Based on stem-loop qRT-PCR, eight miRNAs were validated. 3. Potential target genes of the abundant miRNAs were predicted, and further Kyoto Encyclopedia of Genes and Genomes database (KEGG) and Gene Ontology (GO) analyses were performed, which revealed that some candidate miRNAs were involved in the spermatogenesis process, spermatozoa epigenetic programming and further embryonic development. 5. GO and KEGG analyses based on mapping genes of expressed piRNAs were performed, which revealed that spermatozoal piRNAs could play important regulatory roles in embryonic development of offspring. 6. The search for endogenous spermatozoa miRNAs and piRNAs will contribute to a preliminary database for functional and molecular mechanistic studies in embryonic development and spermatozoa epigenetic programming.

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MiR-146a regulates PM -induced inflammation via NF-κB signaling pathway in BEAS-2B cells.

Exposure to particulate matter (PM) leads to kinds of cardiopulmonary diseases, such as asthma, COPD, arrhythmias, lung cancer, etc., which are related to PM-induced inflammation. We have found that PM (aerodynamics diameter <2.5 µm) exposure induces inflammatory response both in vivo and in vitro. Since the toxicity of PM is tightly associated with its size and components, PM (aerodynamics diameter <1.0 µm) is supposed to be more toxic than PM . However, the mechanism of PM -induced inflammation is not clear. Recently, emerging evidences prove that microRNAs play a vital role in regulating inflammation. Therefore, we studied the regulation of miR-146a in PM -induced inflammation in human lung bronchial epithelial BEAS-2B cells. The results show that PM induces the increase of IL-6 and IL-8 in BEAS-2B cells and up-regulates the miR-146a expression by activating NF-κB signaling pathway. Overexpressed miR-146a prevents the nuclear translocation of p65 through inhibiting the IRAK1/TRAF6 expression, and downregulates the expression of IL-6 and IL-8. Taken together, these results demonstrate that miR-146a can negatively feedback regulate PM -induced inflammation via NF-κB signaling pathway in BEAS-2B cells.

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