MicroRNA expression profile in HEK293T cells infected with Chikungunya virus
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Dr. Ritu Kulshreshtha
PROVIDER: E-GEOD-49884 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:HEK293T grown in 6 well plates were infected with CHIKV and total RNA was isolated from cells at 0, 12 and 24 hrs post infection. CHIKV gene expression signature was generated. Cells grown on 6-well plates. Three biological replicates of uninfected and two biological replicates of infected samples
2014-01-20 | E-GEOD-49985 | biostudies-arrayexpress
Project description:HEK293T grown in 6 well plates were infected with CHIKV and total RNA was isolated from cells at 0, 12 and 24 hrs post infection. CHIKV microRNA expression signature was generated.
2014-01-01 | GSE49884 | GEO
Project description:HEK293T grown in 6 well plates were infected with CHIKV and total RNA was isolated from cells at 0, 12 and 24 hrs post infection. CHIKV gene expression signature was generated.
2014-01-20 | GSE49985 | GEO
Project description:Infection with antimony resistant (SbR) but not with sentitive (SbS) Leishmania donovani (LD) gives rise to aggressive pathology in mammalian hosts, the cause of which is far from clear. Some intracellular pathogens exploit autophagy for their own benefit. Here we show that induction of autophagy in normal macrophages (MF) by pharmacological mediators prior to infection with SbRLD (SbRLD-MF) enhanced their growth as compared to untreated MF, unlike SbSLD-MF. Autophagy was evident in SbRLD-MF from electron microscopical studies showing double membrane-bound compartment around amastigote. In SbRLD-MF there is induction of beclin 1, which forms the platform to recruit other interacting molecules to initiate autophagy. Knocking down the beclin 1 transcription factor Nrf2 and subsequent infection with SbRLD showed significantly lower organ parasites as compared to wild type BALB/c mice. Cessation of autophagy in SbRLD-MF at the later stage of infection is coupled with induction of miR-30a, whose binding to 3'UTR of beclin 1 leads to its post-transcriptional attenuation followed by rise in intracellular Ca++ and apoptosis. SbRLD mediated translocation of AP-1 transcription factor to the nucleus induce pri-miR-30a over-expression. Rise in Ca++ causes caspase 8 activtion leading to the cleavage of beclin 1 and initiation of apoptosis in SbRLD-MF. Apoptosis may favor parasite egress for cell to cell transmission. We also found that beclin 1 expression is present in splenocytes of kala-azar patients harbouring SbRLD but not SbSLD. Our results suggest that SbRLD has evolved a unique mechanism for its own benefit which explains, in part, the cause of aggressive pathology. Peritoneal exudate macrophages were isolated from mouse, grown in 60mm plates and infected with Leishmania donovani and total RNA was isolated from cells at 12, 18 and 24 hrs post infection. Leishmania infected macrophage miRNA expression signature was generated. Cells grown on 60mm plates and infected with Leishmania. The main objective of the microarray analysis of mmu-miRNA in antimony resistant and antimony sensitive Leishmania donovani infected macrophages are as follows: 1. To study how the expression of miRNA varies in either antimony resistant or antimony sensitive Leishmania infected macrophages as compared to the normal macrophages as a function of time. LPS was used as control. 2. To study the expression of those miRNAs which are differentially expressed in antimony resistant and antimony sensitive Leishmania infected macrophages at each time point post infection. 3. To identify those miRNAs which are responsible for degradation of autophagy initiating protein beclin 1 mRNA
2014-04-25 | E-GEOD-57042 | biostudies-arrayexpress
Project description:Global microarray was performed from Trans-Iliac Bone biopsy from the patient with clinically characterized Fibrogensis imperfecta ossium (FIO). A 40-year-old male patient with clinically characterized Fibrogensis imperfecta ossium (FIO) includes fragility fracture with osteomalacia (Losserâ??s zone). On examination, his height was 158 cm, weight 47 kg, body mass index (BMI) 16.5, and his blood pressure was 120/80 mmHg. He had no palpable goiter, neck masses or lymphadenopathy. He had no exostosis or bony deformity. He had difficulty in getting up from squatting position and needed a stick to help with walking. The hip joint movements were painful and restricted.. The rest of the examination including abdomen was other wise normal or non-contributory. His laboratory evaluation was as follows: hemoglobin 13.2gm/dl, total WBC 7200/mm3 and erythrocyte sedimentation rate12 mm for 1st hour. Mean ± SD (3 values) serum calcium (Ca) adjusted for albumin was 9.5 ± 1.3 mg/dl (reference range: 8.5 - 11mg/dl). Serum phosphate (PO4) was 3.5 ± 0.3 mg/dl (reference range 3.5-5.0 mg/dl), serum magnesium 1.6mg/dl (reference range 1.58-2.55 mg/dl), total alkaline phosphatase (AP) 39.6 ± 2.6 KA Units (reference range: 3 â?? 13 KA Units), serum creatinine (Cr) was 1.1 mg/dl. Liver function tests were normal. Twenty four hour mean urine Ca, and phosphorus was 65.3 and 563 mg/d, respectively. The renal tubular handling of phosphate was normal (TmP/GFR 4.2 mg/dl â?? normal 2.4-4.2). The serum intact parathyroid hormone (iPTH) level by immunochemilunometry was 19 pg/ml (reference range: 10-69 pg/ml).Serum 25-hydroxyvitamin D level was 59.9( reference range 9 â?? 37 ng/ml). Serum 1,25-hydroxyvitamin D level was 76.6 ng/ml (reference range â?? 3 ng/ml). Arterial blood gases and urine pH were within normal range. Thyroid function tests were normal. Serum tissue transglutaminase antibody (tTG) titre was negative. Urine for Bence Jones protein was negative and serum electrophoresis was normal. Radiographs of the skull and hands were normal. The lumbar spine showed â??rugger â??jerseyâ?? spine with osteopenia . Views of the pelvis showed bilateral coxa vera and bilateral femur neck fracture with â??fishnet appearanceâ??. The chest radiograph showed multiple Looser zones with fractures of several ribs. The lower end of tibia showed â??fishnet appearanceâ??, tendon calcification and new bone formation. Ultrasonography of the neck did not reveal any abnormality in the thyroid or parathyroid glands. Ultrasonography of the abdomen and KUB region was normal. A 99mTc sestamibi scan was normal. Bone mineral density (BMD) of the hip with a T-score of -2.2 SD. Magnetic resonance imaging of pelvis showed fracture of bilateral neck and hypointense marrow on T1W and T2W sequences . A 99mTc MDP bone scan showed increased radiotracer uptake bilaterally in the shoulders, elbows, wrists, small joints of hands, multiple sites at bilateral ribs, the entire vertebral column, and lower end of tibia but not the skull (beheaed scan). Transiliac bone biopsy showed thickened bony trabeculae with obliteration of marrow spaces and at places, focal areas of exaggerated osteoclastic activity. There was prominent osteoblastic proliferation as well as osteoid like areas were also seen. At places it showed sclerosis, eaten up edges of bone and foci of new calcification (bone formation). With the above mentioned clinical and investigation proile a diagnosis of FIO was considered most likely FIO may easily be misdiagnosed because of its superficial similarity to axial osteomalacia osteoporosis, and other metabolic bone disorders with pathological fractures. Bone pain or pathological fractures in a previously healthy adult should lead to radiological and biochemical investigation. Generalized increase in radiological bone density may indicate myelofibrosis or fluorosis but an increased level of alkaline phosphatase favours Pagetâ??s disease or osteomalacia. Bone biopsy suggests gross osteomalacia until the nostic process is rarely logical, but it would not be so delayed if bone sections were always examined under polarized light. There are many unsolved problems in this crippling condition. Apart from complete ignorance of the cause, yet it is not known, what is replacing the mature collagen of bone, why other collagen-containing tissues are apparently unaffected. Why patients commonly have circulating paraprotein and whether there is any effective treatment. Till date, there is no literature has been reported exploring the genes involved in the pathogenesis of FIO. Hence, aim of present study is identification of various genes involved in the regulation of various signaling pathways involved in pathogenesis of FIO. Total RNA was isolated from Trans-Iliac Bone biopsy (Control Individual (n=1) & Patient (n=1)) using TRIZOL method and global microarray was performed on Affymetrix Genechip HumanPrimview platform. The array was performed on duplicate.
2016-07-31 | E-GEOD-43861 | biostudies-arrayexpress
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
2015-01-01 | E-GEOD-57550 | biostudies-arrayexpress
Project description:Percutaneous coronary intervention (PCI) with stent placement is a standard treatment for coronary artery disease (CAD). Despite all medical advances, restenosis remains a challenging clinical problem. However, the molecular and biochemical pathways of restenotic process are not fully understood yet. Furthermore, as restenosis is assumed to be a multigenetic process and genetic predisposition is considered an important risk factor, analysis of the genome-wide gene expression is recommended for better insight of the phenomenon. We used microarray technology to monitor thousands of genes expression simultaneously. The whole genome expression will be analyzed with this technique to identify cluster of up-regulated and down-regulated genes which may be involved in this complex pathological condition. Coronary restenosis after percutaneous coronary intervention remains a challenging problem, despite all medical advances. Molecular and biochemical pathways of restenotic process are not fully understood yet. Furthermore, as restenosis is assumed to be a multigenetic process. We used microarray technology to monitor thousands of genes expression simultaneously in restenosis postive group with reference restenosis negative group, which will unravel potentially modifiable pathways, possible targets and biomarkers for coronary restenosis.
2014-04-30 | E-GEOD-46560 | biostudies-arrayexpress
Project description:CHME3 cells grown on six-wells were infected with Japanese encephalitis virus (JEV) (P20778 strain ) and total RNA was isolated from cells at 6, 24 and 48 h of post infection mRNA expression was significantly altered in JEV infected human microglial cells. A time dependant change in microRNA profile was noted. Bioinformatics analysis identified anti correlation between differentially expressed miRNAs and the gene expression at different time point which ultimately affected several signalling pathways in microglia cells. Brain enriched microRNAs and a set of microRNA previously designated as NeurimmiRs were also differentially expressed in response to JEV infection Cells grown on 6-well well plate. Three replicates of uninfected and infected samples at each time point was used for mRNA experiment.
2015-01-01 | E-GEOD-57330 | biostudies-arrayexpress
Project description:We report bulk RNA-sequencing from a HEK293T cell line grown under normal conditions.
2021-10-22 | GSE186192 | GEO
Project description:To evaluate the effect of mouse Siglec1 on B16F10 melanoma we used co-culture methos where HEK293T cells were transiently transfected with plasmid containg mouse Siglec1 or empty plasmid (mock). These HEK293T cells were cultured with B16F10-GFP mouse melanoma cells for 18 hours in low binding plates. After 18 hours of incubation on 37°C, 5% CO2, melanoma cells were FACS sorted based on GFP expression and total RNA was isolated and used for TruSeq RNA library construction for transcriptome analysis. Samples were from 3 independent experiments. The library preparation and NGS data aquisition were performed by Macrogen (Macrogen, Inc., Korea)
2019-12-22 | GSE109077 | GEO