ABSTRACT: We characterised and compared the microRNA profiles of the hippocampus tissues from experimental and control groups. The rats in experimental group were exposed to flurothyl and presented recurrent seizure phenotype. The control group were exposed to solvent. There are three tissue samples in each group. 2 out of 3 samples in each group has raw data. 1 out of 3 samples in each group has exported txt file data from the raw data due to technical issues.
Project description:Purpose: To identify tissue microRNAs predictive of sunitinib activity in patients with metastatic renal-cell carcinoma (MRCC) and to validate them in a cellular model. Selected microRNAs were studied in serum from MRCC patients and healthy individuals. Methods: We screened 673 microRNAs using TaqMan Low-density Arrays (TLDAs) in tumors from MRCC patients with extreme phenotypes of marked efficacy and resistance to sunitinib, selected from an identification cohort (n=41). Differentially expressed microRNAs were selected using bioinformatics-based target prediction analysis and quantified by qRT-PCR in tumors from patients presenting similar phenoytpes selected from an independent cohort (n=117). Results were validated in a cellular model of sunitinib resistance and studied in serum from healthy individuals and MRCC patients. Results: TLDAs identified 64 microRNAs differentially expressed in the identification cohort. Seven candidates were quantified by qRT-PCR in the independent series. MiR-942 was the most accurate predictor of sunitinib efficacy (p=0.0074). High expression of miR-942, miR-133a, miR484, and miR-628-5p was significantly associated with decreased time-to-progression and overall survival. These microRNAs were overexpressed in the sunitinib resistant cell line Caki-2 in comparison with the sensitive parental cell line. Serum levels of miR-942, miR-133a, miR-484, miR-146a-5p, miR-374a and miR-486-5p were significantly reduced in MRCC patients compared to healthy controls. Conclusions: Our strategy identified differentially expressed microRNAs in MRCC patients presenting marked sensitivity and resistance to sunitinib. Mir-942 was the best predictor of efficacy. Results were confirmed in a cellular model of sunitinib resistance. We also identified exosome derived serum microRNAs differentially expressed in MRCC patients and healthy individuals. Taqman Low Density Array for 6 FFPE tissues obtained from extreme phenotype MRCC patients, (n=3 marked resistance to sunitinib treatment patients and n=3 marked sensitivity to sunitinib treatment patients), was performanced to screen 667 microRNAs.
Project description:We determined expression profiles of 667 miRNAs using TaqMan Low Density Arrays (TLDA-TaqMan Array Human MicroRNA Card Set v2.0, Applied Biosystems) in 8 samples of colorectal cancer tissues and 8 samples of paired non-tumoral colonic tissues.
Project description:This study describes differential miRNA expression in small intestinal lamina propria leukocyte samples longitudinally during the course of SIV infection of rhesus macaques. Notably, the T-cell activation associated miR-15b, miR-142-3p, miR-142-5p and miR-150 expression was significantly downregulated at 90 and 180DPI. Further, reporter and overexpression assays validated IRAK1 as a direct miR-150 target. Furthermore, IRAK1 protein levels were markedly elevated in intestinal LPLs and epithelium. Finally, blockade of CD8+ T-cell activation/proliferation with delta-9 tetrahydrocannabinol (ï9-THC) significantly prevented miR-150 downregulation and IRAK1 upregulation. Our findings suggest that miR-150 downregulation during T-cell activation may disrupt the translational control of IRAK1 facilitating persistent GI inflammation. We performed TaqMan Low Density Array based high throughput miRNA analysis on small intestine tissue from 12 chronically SIV-infected and 4 uninfected control macaques. All SIV-infected animals were inoculated intravenously with 100TCID50 of SIV. Out of the ten, one animal each was at 7, 8 and 10DPI (days post infection), 3 each at 13 and 21DPI, and 1 at 29DPI. microRNA reverse transcription and preamplification was performed according to the manufacturerâs recommendation. Data analysis was performed using RQ Manager 1.2.2 and DataAssist v3.01 software. Data was normalized using Global normalization method and multiple comparisons correction was performed using Benjamini-Hochberg method.
Project description:The study sought to determine the global miRNA profile of ventricles during early and end-stage hypertrophic cardiomyopathy in a severe double mutant mouse model of the disease. MicroRNA expression profiles of ventricles of transgenic mice with a mutation in both the myosin heavy chain gene (MYH7 Arg403Gln) and cardiac troponin I gene (TNNI3 Ser203Gln) and of non-transgenic mice were determined using Rodent TaqMan Low Density miRNA Arrays A v2.0 (TLDA, Life Technologies). MicroRNA profiles were measured at 10 days of age and 16 days of age, in 3 biological replicates. qRT-PCR analysis of microRNAs of ventricles of three transgenic mice and three non-transgenic mice age 10 days, and three transgenic mice and three non-transgenic mice age 16 days. 450 ng RNA was reverse transcribed, without pre-amplification, using TaqMan MicroRNA Reverse Transcription Kit and Megaplex RT Primers rodent pool A (Life Technologies). Complementary DNA (cDNA) was amplified using a TaqMan rodent microRNA A Array v2.0 (Life Technologies) with TaqMan Universal PCR Master Mix on an ABI 7900HT Sequence Detection System.
Project description:We performed systematic comparison of the miRNA expression profiles between FF and macrodissected FFPE tonsillar tumors using the TaqMan Low Density Array system, with the data processed by different software programs and two types of normalization methods.
Project description:RNA samples were prepared from freshly sorted mammary cell subpopulations (MaSC/basal-enriched, luminal progenitor, mature luminal and stromal) from five sets of adult mice. High throughput RT-PCR was used to measure the global microRNA expression profiles of each cell subpopulation. The expression profiles were compared between cell subpopulations to gain insight into the regulation of lineage-restricted genes. High throughput RT-PCR profiling of microRNA expression in four mouse mammary cell populations. Samples were collected from pooled mammary gland tissue from a number of mice. Samples were collected at over five different times with tissue from independent sets of mice.
Project description:RNA samples were prepared from freshly sorted mammary cell subpopulations (MaSC/basal-enriched, luminal progenitor, mature luminal and stromal) from five human donors. High throughput RT-PCR was used to measure the global microRNA expression profiles of each cell subpopulation. The expression profiles were compared between cell subpopulations to gain insight into the regulation of lineage-restricted genes. High throughput RT-PCR profiling of microRNA expression in four mammary cell populations from five human donors.
Project description:This study sought to determine the dynamic changes of miRNA expression during mouse granulopoiesis. We not only performed analyses of miRNA expression levels in whole cells but also analyzed purified nuclear and cytoplasmic cell fractions to profile miRNA subcellular localization. qRT-PCR analysis of miRNAs was performed on whole cell, nuclear and cytoplasmic RNAs extracted from mouse hemopoietic stem cells (LSKs), promyelocytes, myelocytes and granulocytes. 100 ng of RNA was reversed transcribed using the Taqman miRNA Reverse Transcription Kit and Megaplex RT Primers rodent pool A and B (Life Technologies). Complementary DNA (cDNA) was amplified using a TaqMan rodent microRNA A and B Array v2.0 (Life Technologies) with TaqMan Universal PCR Master Mix on an ABI 7900HT Sequence Detection System.
Project description:Neuroblastoma (NB) is an embryonic tumor arising from immature sympathetic nervous system progenitor cells. MYCN and ALK are driver oncogenes both of which are specifically expressed during early neurogenesis. This is in line with the assumption that NB arises through disruption of normal developmental processes. MYCN has a broad impact on the tumor phenotype; however, the details of the MYCN driven oncogenic program are far from clear. In recent studies we demonstrated that MYCN drives the expression of a defined set of miRNAs that tightly control the expression of several key MYCN target genes, including several components of the TGFβ signaling pathway. In order to gain further insight into the role of miRNAs in NB initiation and progression, we evaluated miRNA profiles of hyperplastic ganglia and tumors isolated from MYCN transgenic mice.