Effect of miR-650 overexpression on gene expression profile of human monocyte-derived dendritic cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Tica Pichulik
PROVIDER: E-GEOD-69228 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Transcriptional profiling of human monocyte-derived dendritic cells, comparing cells transfected for 24h with Pre-miR-650 or nonsense control.
2015-05-27 | GSE69228 | GEO
Project description:Over the last decade, small noncoding RNA molecules such as microRNAs (miRNAs) have emerged as critical regulators in the expression and function of eukaryotic genomes. It has been suggested that viral infections and neurological disease outcome may also be shaped by the influence of small RNAs. This has prompted us to suggest that HIV infection alters the endogenous miRNA expression patterns, thereby contributing to neuronal deregulation and AIDS dementia. Therefore, using primary cultures and neuronal cell lines, we examined the impact of a viral protein (HIV-1 Tat) on the expression of miRNAs due to its characteristic features such as release from the infected cells and taken up by noninfected cells. Using microRNA array assay, we demonstrated that Tat deregulates the levels of several miRNAs. Interestingly, miR-34a was among the most highly induced miRNAs in Tat-treated neurons. Tat also decreases the levels of miR-34a target genes such as CREB protein as shown by real time PCR. The effect of Tat was neutralized in the presence of anti-miR-34a. Using in situ hybridization assay, we found that the levels of miR-34a increase in Tat transgenic mice when compared with the parental mice. Therefore, we conclude that deregulation of neuronal functions by HIV-1 Tat protein is miRNA-dependent. Human neurons SH-SY5Y were chosen to examine the impact of HIV-1 Tat protein on gene expression
2013-01-17 | E-GEOD-43534 | biostudies-arrayexpress
Project description:Over the last decade, small noncoding RNA molecules such as microRNAs (miRNAs) have emerged as critical regulators in the expression and function of eukaryotic genomes. It has been suggested that viral infections and neurological disease outcome may also be shaped by the influence of small RNAs. This has prompted us to suggest that HIV infection alters the endogenous miRNA expression patterns, thereby contributing to neuronal deregulation and AIDS dementia. Therefore, using primary cultures and neuronal cell lines, we examined the impact of a viral protein (HIV-1 Tat) on the expression of miRNAs due to its characteristic features such as release from the infected cells and taken up by noninfected cells. Using microRNA array assay, we demonstrated that Tat deregulates the levels of several miRNAs. Interestingly, miR-34a was among the most highly induced miRNAs in Tat-treated neurons. Tat also decreases the levels of miR-34a target genes such as CREB protein as shown by real time PCR. The effect of Tat was neutralized in the presence of anti-miR-34a. Using in situ hybridization assay, we found that the levels of miR-34a increase in Tat transgenic mice when compared with the parental mice. Therefore, we conclude that deregulation of neuronal functions by HIV-1 Tat protein is miRNA-dependent. Using primary cultures and neuronal cell lines, we examined the impact of a viral protein (HIV-1 Tat) on the expression of miRNAs and mRNAs.
2013-02-12 | E-GEOD-44265 | biostudies-arrayexpress
Project description:Studies have shown that HIV-infected patients develop neurocognitive disorders characterized by neuronal dysfunction. The lack of productive infection of neurons by HIV suggests that viral and cellular proteins, with neurotoxic activities, released from HIV-1-infected target cells can cause this neuronal deregulation. The viral protein R (Vpr), a protein encoded by HIV-1, has been shown to alter the expression of various important cytokines and inflammatory proteins in infected and uninfected cells; however the mechanisms involved remain unclear. Using a human neuronal cell line, we found that Vpr can be taken up by neurons causing: (i) deregulation of calcium homeostasis, (ii) endoplasmic reticulum-calcium release, (iii) activation of the oxidative stress pathway, (iv) mitochondrial dysfunction and v- synaptic retraction. In search for the cellular factors involved, we performed microRNAs and gene array assays using human neurons (primary cultures or cell line, SH-SY5Y) that we treated with recombinant Vpr proteins. Interestingly, Vpr deregulates the levels of several microRNAs (e.g. miR-34a) and their target genes (e.g. CREB), which could lead to neuronal dysfunctions. Therefore, we conclude that Vpr plays a major role in neuronal dysfunction through deregulating microRNAs and their target genes, a phenomenon that could lead to the development of neurocognitive disorders. Human neurons SH-SY5Y were chosen to examine the impact of HIV-1 Vpr protein on gene expression
2013-01-17 | E-GEOD-43535 | biostudies-arrayexpress
Project description:Studies have shown that HIV-infected patients develop neurocognitive disorders characterized by neuronal dysfunction. The lack of productive infection of neurons by HIV suggests that viral and cellular proteins, with neurotoxic activities, released from HIV-1-infected target cells can cause this neuronal deregulation. The viral protein R (Vpr), a protein encoded by HIV-1, has been shown to alter the expression of various important cytokines and inflammatory proteins in infected and uninfected cells; however the mechanisms involved remain unclear. Using a human neuronal cell line, we found that Vpr can be taken up by neurons causing: (i) deregulation of calcium homeostasis, (ii) endoplasmic reticulum-calcium release, (iii) activation of the oxidative stress pathway, (iv) mitochondrial dysfunction and v- synaptic retraction. In search for the cellular factors involved, we performed microRNAs and gene array assays using human neurons (primary cultures or cell line, SH-SY5Y) that we treated with recombinant Vpr proteins. Interestingly, Vpr deregulates the levels of several microRNAs (e.g. miR-34a) and their target genes (e.g. CREB), which could lead to neuronal dysfunctions. Therefore, we conclude that Vpr plays a major role in neuronal dysfunction through deregulating microRNAs and their target genes, a phenomenon that could lead to the development of neurocognitive disorders. Using primary cultures and neuronal cell lines, we examined the impact of a viral protein (HIV-1 Vpr) on the expression of miRNAs and mRNAs.
2013-02-12 | E-GEOD-44266 | biostudies-arrayexpress
Project description:HEK293 cells were transfected with control plasmid (pcDNAI/Neo;Invitrogen) or with the plasmid encoding HCaRG. Stable transfectants were synchronized and grown in the presence of 10% FBS for 48 h. Total RNAs were purified with the mini RNeasy kit (Qiagen). Chips: HG-U133A; - Labeling protocol: Enzo BioArray HighYield RNA Transcript Labeling Kit. - Hybridization: According to the manufacturer's protocol (Affymetrix). - Scanner: GeneArray 2500. - Normalization: Employing GCOS software, chips were normalized using all probe sets scaling option and target signal at 500. Chips: HG-U133 Plus 2.0; - Labeling protocol: GeneChip IVT Labeling Kit. - Hybridization: According to the manufacturer's protocol (Affymetrix). - Scanner: GeneChip Scanner 3000. - Normalization: Employing GCOS software, chips were normalized using all probe sets scaling option and target signal at 500.
2007-09-07 | E-GEOD-2555 | biostudies-arrayexpress
Project description:CONTEXT Nowadays, the molecular mechanisms involved in endometrial receptivity and implantation are still not clear. OBJECTIVE The gene expression of human endometrium of patients undergoing an IVF treatment with GnRH antagonists/rec-FSH was studied. CONCLUSIONS COX-2 has been extensively studied as a crucial fertility element in both knock-out mice and human. It appears that increased expression of COX-2 and/or SCGB1D2 on the day of oocyte retrieval in GnRH antagonist/rec-FSH stimulated cycles coincides with a lower probability of achieving a clinical pregnancy in this cycle. Keywords: gene expression analysis, clinical pregnancy in IVF stimulated cycles Endometrial biopsies taken from patients on day of oocyte retrieval in stimulated IVF cycles with 1 or 2 embryos replaced in the same cycle. Gene expression of pregnant patients (n=4) was compared with matched non-pregnant patients (n=4)
2010-09-06 | E-GEOD-18140 | biostudies-arrayexpress
Project description:Analysis of acute myeloid leukemia KG1 cells treated with XX-650-23 (5 mM) for 12hrs. XX-650-23 inhibits proliferation of KG1 cells. Results provides insight into the molecular mechanisms underlying by the inhibitory activity of XX-650-23 on acute leukemia.
2016-03-26 | GSE74928 | GEO
Project description:Analysis of acute myeloid leukemia KG1 cells treated with XX-650-23 (5 mM) for 12hrs. XX-650-23 inhibits proliferation of KG1 cells. Results provides insight into the molecular mechanisms underlying by the inhibitory activity of XX-650-23 on acute leukemia. mRNA profiles of KG1 cells treated with XX-650-23 were generated by deep sequencing. CREB genome binding profiles of KG1 cells treated with XX-650-23 were generated by deep sequencing.
2016-03-26 | E-GEOD-74928 | biostudies-arrayexpress
Project description:Reproductive barriers perform a vital role during speciation1. Hybrid weakness, the poor development of hybrids compared to their parents, hinders gene exchange between different species at the postzygotic stage2,3. The molecular and evolutionary mechanisms of hybrid weakness are poorly understood2. Here, we report that two incompatible dominant loci (Hwi1 and Hwi2) involving three genes determine the high temperature-dependent expression of hybrid weakness in interspecific hybrids of rice. Hwi1 comprises two indispensable wild rice (Oryza rufipogon)-specific leucine-rich repeat receptor-like kinase (LRR-RLK) genes, 25L1 and 25L2, for inducing hybrid weakness, and the genes possibly undergo balancing selection. Hwi2, a rare allele that is predominantly distributed in indica rice (Oryza sativa), encodes a secreted putative subtilisin-like protease. Functional analysis indicated that pyramiding of Hwi1 and Hwi2 activates the autoimmune response in the basal nodes of hybrids, interrupting root formation and then impairing shoot growth, likely due to immune signal is transmitted from the basal nodes to the above-ground parts. Considering the nature of RLK activity of Hwi1 and the protease activity of Hwi2, we propose that a certain endogenous signaling molecule produced by Hwi2 is perceived by Hwi1 to activate autoimmunity through ligand-receptor signal transduction. These findings bring new insights into our understanding of reproductive isolation and may benefit rice breeding to maximally utilize invaluable genes from wild rice. We conducted microarray analysis to unravel the global changes in gene expression of a pair of NILs (nearly isogenic lines). Plants were cultivated at constant 20°C for 20 days and then shifted to constant 30°C conditions. The basal nodes of NIL(Hwi1) and NIL(hwi1) were harvested immediately before the temperature shift (set as the 0 point) or at 3, 7 or 15 days after the shift. Three biological replicates (each comprising basal nodes from 15–20 individuals) were used for each time point.
2014-01-22 | E-GEOD-54243 | biostudies-arrayexpress