Project description:The effect of PDGF-DD on the gene expression of human tonsil ILC1 is unknown. We used microarray to determine the transcriptional differences between unstimulated and PDGF-DD-stimulated human tonsil ILC1.
Project description:To investigate miRNA expression in human tonsil squamous cell carcinoma (SCC) compared to normal tonsil tissue. Two colour LNA Exiqon array. MicroRNAs were labeled at 3'-end with a P-CU-C3-Cy3 RNA linker. A mixture of 371 synthetic DNA reference oligonucleotides containing complementary sequences to all LNA probes was randomly labeled using the ULYSIS labeling kit.
Project description:B cells from human tonsil and blood were sorted using flow cytometry. The human samples were processed immediately ex-vivo using markers for known B cell subsets.
Project description:Innate lymphoid cell (ILC) subsets that mirror helper T cells in their effector cytokine profiles have recently emerged as central players in both homeostatic and inflammatory conditions. Like their Th1, Th2 and Th17/Th22 helper T cell counterparts, ILC subsets are categorized based on their expression of specific transcription factors and effector cytokines: group 1 ILC (ILC1) express T-bet and IFN-γ; group 2 ILC (ILC2) express GATA-3 and type 2 effector cytokines such as IL-13 and IL-5; and group 3 ILC (ILC3) express RORgt and the cytokines IL-22 and/or IL-17. Under this nomenclature, natural killer (NK) cells and lymphoid tissue inducers (LTi) are considered ILC1 and ILC3, respectively. ILC1 contain both CD4+ and CD4- populations, but whether this phenotypic characteristic reflects functional differences between these two populations is unknown. These studies examine the gene expression profiles of CD4+ vs CD4- ILC1 in a cohort of healthy control subjects. ILC subsets were isolated from the peripheral blood of healthy control subjects. cDNA was isolated and amplified from sorted populations, and gene expression was analyzed by RNAseq
Project description:Transcriptional profiling of human glioma cells comparing control GFP expressing cells with glioma cells transfected with a human PDGF-A gene. The isogenic cell lines were used to study the impact on glioma tumorigenesis and invasion. Goal was to determine the effects of PDGF-A gene transfection on global ES gene expression. Two set of glioma cell lines, LN444 vs LN444/PDGF-A and LN443 vs LN443/PDGF-A. Biological replicates: 2 control replicates, 2 transfected replicates.
Project description:Single cell RNA-sequencing of human tonsil Innate lymphoid cells (ILCs) from three independent tonsil donors. Sequencing libraries were prepared from FACS sorted individual ILCs with the Smart-Seq2 protocol (Picelli et al. Nature Methods 2013)
Project description:Transcriptional profiling of human glioma cells comparing control GFP expressing cells with glioma cells transfected with a human PDGF-A gene. The isogenic cell lines were used to study the impact on glioma tumorigenesis and invasion. Goal was to determine the effects of PDGF-A gene transfection on global ES gene expression.
Project description:Platelet-derived growth factor-CC (PDGF-CC) is the third member of the PDGF family discovered after more than two decades of studies on the original members of the family, PDGF-AA and PDGF-BB. The biological function of PDGF-CC remains largely to be explored. We report here a novel finding that PDGF-CC is a potent neuroprotective factor that acts by modulating glycogen synthase kinase (GSK)3beta activity. In several different animal models of neuronal injury, such as axotomy-induced neuronal death, neurotoxin-induced neuronal injury, 6-OHDA-induced Parkinson's dopaminergic neuronal death and ischemia-induced stroke, PDGF-CC protein or gene delivery protected different types of neurons from apoptosis in both the retina and brain. On the other hand, loss-of-function assays using PDGF-C null mice, neutralizing antibody or shRNA showed that PDGF-CC deficiency/inhibition exacerbated neuronal death in different neuronal tissues in vivo. Mechanistically, we revealed that the neuroprotective effect of PDGF-CC was achieved by regulating GSK3beta phosphorylation and expression. Our data demonstrate that PDGF-CC is critically required for neuronal survival, and may potentially be used to treat neurodegenerative diseases. Inhibition of the PDGF-CC/receptor pathway for different clinical purposes should be conducted with caution to preserve normal neuronal functions.