Project description:The goal of this study was to identify chromatin regulatory sites by FAIRE-seq under conditions of basal and increased dosage of transcription factor SF-1 in the H295R human adrenocortical tumor cell line. 4 samples: input DNA in basal SF-1 expression conditions - FAIRE-seq in basal SF-1 expression conditions - input DNA in SF-1 overexpression conditions - FAIRE-seq in SF-1 overexpression conditions
Project description:The goal of this study was to identify genomic binding sites of the NRSF/REST transcription factor under conditions of basal and increased SF-1 dosage in the H295R human adrenocortical tumor cell line. 4 samples: input DNA (2 replicates) - NRSF/REST ChIP basal SF-1 dosage - NRSF/REST ChIP increased SF-1 dosage
Project description:Analysis of smallRNA in THP1 (human monocytic leukemia) cell line in order to correlate miRNA activity with target abundance. THP1 smallRNA profiles were generated in triplicates by deep-sequencing in Illumina HiSeq2000.
Project description:Macrophages have plasticity to adapt microenvironment. In joint tissue, synovial macrophages (SM) and synovial fibroblasts (SF) are maintained in the homeostasis. In Rheumatoid arthritis, crosstalk between SM and SF via inflammatory response induce abnormal activation in respective cells and contribute to disease progression. However, the activation mechanisms in SM which are encouraged by SF are largely unclear. Here, we demonstrated metabolic reprogramming and immunological activation in SM by secretary stimulations from SF using primary culture synovial cell derived from arthritis model mice. To analyze interaction between SM and SF, primary culture of murine synovial cells was performed, respectively. RNA-seq analysis showed SF express abundant secretion-related gene. Thus, we investigated whether conditioned medium from SF (SF-CM) affects biological activity in SM. As the results, SF-CM condition induced both glycolysis and mitochondrial respiration to SM with increased uptake of glucose and glutamine at least, accompanied with cell survival. In addition, several inflammation markers were also upregulated in SM by SF-CM condition. Taken together, these results suggest that metabolic reprogramming were induced in SM by secretory stimulations from SF, followed by activated inflammatory response and long-live. These indicate that such phenotypes of SM may contribute to chronic inflammation in Rheumatoid arthritis