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Literatura académica sobre el tema "MiR-544a"

Autor: Grafiati

Publicado: 14 de marzo de 2023

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Artículos de revistas sobre el tema "MiR-544a"

Yang, Lei, Dawei Ge, Xi Chen, Chunzhi Jiang y Shengnai Zheng. "miRNA-544a Regulates the Inflammation of Spinal Cord Injury by Inhibiting the Expression of NEUROD4". Cellular Physiology and Biochemistry 51, n.º 4 (2018): 1921–31. http://dx.doi.org/10.1159/000495717.

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Background/Aims: To explore the potential role of miR-544a in spinal cord injury and the possible mechanism involved. Methods: We established a mouse model with spinal cord injury to examine the changes in grip force recovery of the forelimb or the posterior limb of the mouse. Microarray was performed to achieve differentiated miRNAs in the mice. The expressions of miR-544a, MCP-1, IL36B and IL17B after spinal cord injury were detected by qRT-PCR. Subsequently, miR-544a was overexpressed to observe changes in inflammation and grip strength after spinal cord injury. Target gene of miR-544a was then predicted using bioinformatics technology. Finally, dual luciferase reporter gene assay was used to verify the binding of miR-544a to its target gene. Results: Using mice models with spinal cord injury, we found that the strength of their four limbs began to recover 7 days after injury. The results of microarray and qRT-PCR confirmed that mir-544a level in mice with spinal cord injury decreased with increase of injury time, while the levels of inflammatory genes MCP-1 (monocyte chemoattractant protein-1), IL1 (interleukin-1) and TNF-α (tumor necrosis factor alpha) IL36B (interleukin-36 beta) and IL17B (interleukin-17 beta) were significantly increased. However, overexpression of miR-544a in the mice significantly reduced the level of inflammation and restored their grip strength in their four limbs. Finally, we found that miR-544a can bind to the NEUROD4 (Neurogenic differentiation 4) 3’UTR (Untranslated Region) region through bioinformatics website prediction, which was further confirmed by dual luciferase reporter assay. NEUROD4 level was significantly reduced following the overexpression of miR-544a. Conclusion: The expression of miR-544a was significantly decreased after spinal cord injury. High expression of miR-544a could alleviate the inflammation caused by spinal cord injury and promote the recovery of spinal cord via the inhibition of NEUROD4.

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Alsaadoni, Hani, Burcu Çaykara, Sadrettin Pençe, Halime Hanım Pençe y Süleyman Bademler. "The expression levels of miR-655-3p, miR127-5p, miR-369-3p, miR-544a in gastric cancer". Turkish Journal of Biochemistry 44, n.º 4 (23 de agosto de 2019): 487–91. http://dx.doi.org/10.1515/tjb-2019-0057.

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Abstract Background Gastric cancer, one of the most common cancers in the world, is a multifactorial disease in which environmental and genetic factors play a role. In our study, we aimed to determine the expression levels of four miRNAs (miR127-5p, miR-544a, miR-369-3p and miR-655-3p) on chromosome 14q32 in gastric cancer. Materials and methods Total RNA was isolated from blood samples taken from 66 gastric cancer and 66 healthy individuals. The gene expression levels determined by cDNA and quantitative real-time polymerase chain reaction were analyzed according to the 2−∆∆Ct method. SPSS 22 were used for statistical analysis and p < 0.05 was considered as statistically significant. Results and discussion miR-655-3p (fold change: 100, p = 0.026), miR-127-5p (fold change: 48, p < 0.001) and miR-369-3p (fold change: 1.6, p > 0.05) was less expressed in the gastric cancer group than control group. miR-544a was found 15.5-fold more expressed in the patient group than control group (fold change: 15.47, p < 0.001). Conclusion miR127-5p, miR-544a, and miR-655-3p may be evaluated as biomarkers in gastric cancer.

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Pan, Lingxiao y Kaifeng Gan. "MiR-544a Regulates Synovial Cell Proliferation, Invasion, Migration and Apoptosis by Targeting E2F2". Journal of Biomaterials and Tissue Engineering 9, n.º 8 (1 de agosto de 2019): 1065–72. http://dx.doi.org/10.1166/jbt.2019.2108.

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In the present study, we aimed to explore the role of MiR-544a in inhibiting the proliferation and promoting apoptosis of rheumatoid arthritis synovial cells. Detected the expression of MiR-544 and E2F2 in Normal Fibroblast-like synoviocytes (NFLs) and Rheumatoid arthritis Fibroblast-like synoviocytes (RA-FLSs) by RT-qPCR and western blot. The target genes of MiR-544a were predicted by miRDB and were verified with the luciferase reporter system and western blot. The E2F2 overexpression plasmid was constructed and transfected into RAFLS. Cell apoptosis were detected by CCK-8. Wound healing and transwell assay were employed to detect cell invasion ability. The expression of E2F2, MMP2 and MMP9 were measured by Western blot. Further, the level of apoptosis and live cells were detected by flow cytometry DAPI staining, respectively. The expression of cell proliferation, apoptosis and migration-related proteins were detected by Western blot. The expression of miR-544 in RA-FLSs is significantly lower than that in NFLs and E2F2 is increased in RA-FLSs. E2F2 is one of the target genes of miR-544a by miRDB detection and luciferase activity assay. Overexpression of miR-544 inhibits cell proliferation, invasion, migration and apoptosis by targeting E2F2 in RA-FLSs. MiR-544a regulates synovial cell proliferation, invasion, migration and apoptosis by targeting E2F2, which is expected to be an attractive target for the development of new drugs for the treatment of rheumatoid arthritis.

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Potenza, Nicoletta, Filomena Castiello, Marta Panella, Giovanni Colonna, Gennaro Ciliberto, Aniello Russo y Susan Costantini. "Human MiR-544a Modulates SELK Expression in Hepatocarcinoma Cell Lines". PLOS ONE 11, n.º 6 (8 de junio de 2016): e0156908. http://dx.doi.org/10.1371/journal.pone.0156908.

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Stella di Stadio, Chiara, Raffaella Faraonio, Antonella Federico, Filomena Altieri, Emilia Rippa y Paolo Arcari. "GKN1 expression in gastric cancer cells is negatively regulated by miR-544a". Biochimie 167 (diciembre de 2019): 42–48. http://dx.doi.org/10.1016/j.biochi.2019.09.005.

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Lu, Pengwei, Yuanting Gu, Lin Li, Fang Wang y Xinguang Qiu. "miR-544a Promotes Breast Cancer Cell Migration and Invasion Reducing Cadherin 1 Expression". Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 23, n.º 4 (25 de marzo de 2016): 165–70. http://dx.doi.org/10.3727/096504016x14519157902726.

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Azari, Hanieh, Elham Karimi, Mohammad Shekari, Ahmad Tahmasebi, Amin Reza Nikpoor, Ahmad Agha Negahi, Nima Sanadgol y Pegah Mousavi. "Construction of a lncRNA–miRNA–mRNA network to determine the key regulators of the Th1/Th2 imbalance in multiple sclerosis". Epigenomics 13, n.º 22 (noviembre de 2021): 1797–815. http://dx.doi.org/10.2217/epi-2021-0296.

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Aim: The exact epigenetic mechanisms that determine the balance of T helper (Th)1 and Th2 cells and autoimmune responses in multiple sclerosis (MS) remain unclear. We aim to clarify these. Methods: A combination of bioinformatics analysis and molecular evaluations was utilized to identify master hub genes. Results: A competitive endogenous RNA network containing six long noncoding RNAs (lncRNAs), 21 miRNAs and 86 mRNAs was provided through enrichment analysis and a protein–protein interaction network. NEAT1 and MALAT1 were found as differentially expressed lncRNAs using Gene Expression Omnibus (GSE21942). Quantitative real-time PCR results demonstrate dysregulation in the RUNX3 (a regulator of Th1/Th2 balance), GATA3 and TBX21, as well as miR-544a and miR-210-3p (which directly target RUNX3). ELISA also confirmed an imbalance in IFN-γ (Th1)/IL-4 (Th2) in MS patients. Conclusion: Our findings introduce novel biomarkers leading to Th1/Th2 imbalance in MS.

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De Palma, A., C. Heluany, A. Fioravanti, I. Clark y G. Nalesso. "MIR-544A: A NEW MODULATOR OF THE WNT/β-CATENIN PATHWAY IN ARTICULAR CHONDROCYTES". Osteoarthritis and Cartilage 30 (abril de 2022): S169. http://dx.doi.org/10.1016/j.joca.2022.02.220.

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Liu, Xiaochun, Jing Ma, Feng Xu y Li Li. "TINCR suppresses proliferation and invasion through regulating miR-544a/FBXW7 axis in lung cancer". Biomedicine & Pharmacotherapy 99 (marzo de 2018): 9–17. http://dx.doi.org/10.1016/j.biopha.2018.01.049.

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He, Qianru, Lini Zhao, Yunhui Liu, Xiaobai Liu, Jian Zheng, Hai Yu, Heng Cai et al. "circ-SHKBP1 Regulates the Angiogenesis of U87 Glioma-Exposed Endothelial Cells through miR-544a/FOXP1 and miR-379/FOXP2 Pathways". Molecular Therapy - Nucleic Acids 10 (marzo de 2018): 331–48. http://dx.doi.org/10.1016/j.omtn.2017.12.014.

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Tesis sobre el tema "MiR-544a"

DE, PALMA ANNA. "First evidences of the role of miR-544a in the modulation of the Wnt signalling in the articular cartilage: potential impact in the pathophysiology of osteoarthritis". Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1072132.

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Background: Osteoarthritis (OA) is the most common degenerative musculoskeletal condition. Progressive degeneration of the articular cartilage is a hallmark of the disease. A better understanding of OA pathogenetic mechanisms is required for the development of disease-modifying drugs capable of stopping disease progression and promoting cartilage repair. MicroRNAs (miRNAs) constitute a class of small noncoding RNAs with an epigenetic role in the negative regulation of gene expression. The differential expression of several miRNAs between healthy and OA cartilage samples highlighted their implication in the pathogenesis of OA. Several molecular pathways are deregulated in the articular cartilage in OA. The involvement of the Wnt/β-catenin pathway in OA pathogenesis is well known, however its role remains controversial, as both its activation or complete inhibition can lead to cartilage degradation and OA. Previous data showed that miR-544a was the most modulated gene by Wnt3a, a Wnt ligand whose expression and activity is modulated in OA. The purpose of this study was therefore to determine the role of miR-544a in the articular cartilage and in the modulation of the Wnt signalling in this tissue. Methodology: Putative target genes of miR-544a were identified through an in silico analysis. Targets related to the Wnt signalling were then further validated by preparation of target-specific luciferase-based reporter assays. The effect of miR-544a on chondrocyte phenotype was investigated by its transient overexpression in the chondrocyte cell line C28/I2 with or without simultaneous stimulation with recombinant Wnt3a. The expression of chondrocyte phenotypic marker genes was assessed by qPCR while proteoglycan synthesis was measured by alcian blue staining on micromass cultures. The effect of pro-inflammatory cytokines on miR-544a expression was finally investigated by gene expression analysis on primary chondrocytes and C28/I2 cell line. Results: Axin2, CDH1, CTNNBIP1 and GSK-3β were confirmed to be target of miR-544a in chondrocytes. The overexpression of miR-544a in C28/I2 cells up-regulated the expression of Col2a1, Aggrecan and MMP-13 and down-regulated ADAMTS-5 and TIMP-3 at mRNA level. These phenotypic effects did not vary in presence of Wnt3a. MicroRNA-544a did not alter proteoglycan content in our culture conditions. IL-6 and TGF-β up-regulated miR-544a expression levels. Conclusion: Our results showed, for the first time, the possible involvement of miR-544a in the modulation of the Wnt signalling in the articular cartilage as well as in the regulation of chondrocyte metabolism. We can speculate that alterations of miR-544a expression levels, which could be induced by pro-inflammatory cytokines during OA, may contribute to a de-regulated activation of the β-catenin-dependent Wnt signalling exacerbating the catabolic activities of chondrocytes and participating to the pathogenesis of OA.

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