Gene expression profiling of SHSY5Y cells exposed to Endosulfan
ABSTRACT: SHSY5Y cells grown in MEM:F12 media (1:1) were treated with Endosulfan and total RNA was isolated from cells after 24 hour exposure Three replicate were used for the experiment Cells grown in 75mm2 flask. three replicates for each sample
Project description:The trace element manganese is essential for normal development for all the organisms. Overexposure of manganese may leads to multiple neuronal disorders such as Parkinson, manganism. To explore the molecular mechanism of manganese induced neurotoxicity, gene expression profiling was performed on human neuroblastoma SHSY-5Y cells. Cells were exposed to sub-lethal concentration of manganese (100 μM) for 24 hrs. Our result demonstrates that manganese alter multiple biological pathways including chromatin assembly, neurogenesis and apoptotic pathways.Cells grown in 75mm2 flask. three replicates for each sample SHSY5Y cells grown in MEM:F12 media (1:1) were treated with manganese and total RNA was isolated from cells after 24 hour exposure Three replicate were used for the experiment
Project description:Long non-coding RNAs (lncRNAs) are a diverse category of transcripts with poor conservation and have expanded greatly in primates, particularly in their brain. We identified a lncRNA, which has acquired 16 microRNA response elements (MREs) for miR-143-3p in the Catarrhini branch of primates. This lncRNA termed LncND (neuro-development) gets expressed in neural progenitor cells and then declines in mature neurons. Binding and release of miR-143-3p, by LncND, can control the expression of Notch. Its expression is highest in radial glia cells in the ventricular and outer subventricular zones of human fetal brain. Down-regulation of LncND in neuroblastoma cells reduced cell proliferation and induced neuronal differentiation, an effect phenocopied by miR-143-3p over-expression and supported by RNA-seq analysis. These findings support a role for LncND in miRNA-mediated regulation of Notch signaling in the expansion of the neural progenitor pool of primates and hence contributing to the rapid growth of the cerebral cortex. SHSY5Y cells treated either with miR-143-3p mimic or 100 nM of siRNA specific for LncND were sequenced on NextSeq500 platform. Scrambled siRNA or miRNA sequences were used as a negative control.
Project description:HepG2 cells grown in DMEM media were treated with 15µM Endosulfan in prescence of S9-mix and total RNA was isolated from cells after 24 hour exposure Cells grown in 75mm2 flask. two replicates for control and two for treatment
Project description:The main scientific objective of the project was to investigate whether Lamin A/C could be involved in neuroblastoma differentiation. Moreover, taking into account the significance of differentiation stage in the neuroblastoma tumor progression we have also studied a possible role of Lamin A/C in the tumorigenesis of this neuronal cancer. As differentiating stimulus we used the all-trans retinoic acid (RA), the most effective compound which has been shown to induce differentiation in neuroblastoma cells. To get insight into the impairment of cell differentiation produced by the LMNA (Lamin A/C) silencing in SHSY5Y cells, we compared the gene expression profile of control and silenced cells both in Retinoic Acid treated and untreated samples, using the one-color Agilent microarray platform. Four condition experiment: cells infected with a mock vector (Mock cells), treated and untreated with retinoic acid (RA); cells infected with a silencing vector for LMNA (LMNA-KD cells), treated and untreated with retinoic acid.
Project description:Fluorosis is caused due to excess of fluoride intake over a long period of time. Aberrant change in RUNX2-mediated signaling cascade is one of the decisive steps during the pathogenesis of fluorosis. Till date, role of fluoride on the epigenetic alterations is not studied. In the present study, global expression profiling ofshort non-coding RNAs, in particular miRNAs and snoRNAs was carried out in NaF treated HOS cells to understand their possible role in the development of fluorosis. RT-PCR and insilico hybridization revealed that miR-124 and miR-155 can be directly involved in the transcriptional regulation of RUNX2 and RANKL genes. Compare to control, C/D box analysis revealed mark elevation in the number of UG dinucleotides and D-box sequences in NaF exposed HOS cells. Herein, we report miR-124 and miR-155 as the new possible players involved in the development of fluorosis. We also state that the alterations in UG dinucleotides and D-box sequences of snoRNAs could be due to NaF exposure. HOS cells grown on MEM media were treated with sodium fluoride and total RNA was isolated from cells after one month of chronic exposure; Cells grown on six 25mm flask. two replicates of control and two different concentration of exposed samples; two replicate are served as control
Project description:To gain an insight into the molecular mechanisms by which bilirubin induces toxicity, we exposed human MCF7 and SHSY5Y cell lines to 50 uM bilirubin (which equates to 6.39 uM of unconjugated bilirubin) for 4 hours. The cells were then washed with PBS and the RNA extracted using Tri-Reagent/1-bromo-3-chloropropane phase separation. The data was extracted using GenomeStudio and normalized/analyzed using ArrayTrack.
Project description:Analysis of knockdown of SDHD with or without knockdown of CDKN1C or SLC22A18 at gene expression level. The hypothesis tested in this study was to determine whether the gene expression signature following SDHD knockdown together with SLC22A18 or CDKN1C more closely resembles the signature found in tumors than the signature resulting from SDHD knockdown alone. Overall design: Total RNA obtained from SNB19 and SHSY5Y cells with single or double knockdown of SDHD and CDKN1C or SLC22A18 compared to scrambled control
Project description:Gene expression profiles of Homarus americanus larvae exposed to five endosulfan concentrations were compared to the control to identify genes that showed significant changes in expression as a result of exposure. There was a significant dose response effect during the endosulfan experiment and changes in gene expression were seen at high endosulfan concentrations that could caused developmental delays and mortality A six condition experiment: control vs 5 endosulfan concentrations. Biological replicates: 6. Array replicates: 1
Project description:Though fluoride is considered an essential trace element, chronic exposure to fluoride is known to cause toxic effects. Chronic exposure of high concentration of fluoride may leads to fluorosis. To understand the molecular mechanism of fluoride induced toxicity gene expression profiling was performed on osteosarcoma cells (HOS). Cells were exposed to sub-lethal concentration of fluoride (8 ppm) for 30 days. Our result demonstrates that fluoride alters multiple biological pathways including bone development, osteoblast differentiation and apoptotic pathways. HOS cells grown in MEM were treated with fluoride and total RNA was isolated from cells after 30 days exposure. Three replicates per group were used for the experiment.