During neonatal development, skeletal muscle grows dramatically by myonuclei accretion to existing fibers and hypertophic growth of fibers with protein synthesis.
An NF-κB--EphrinA5-Dependent Communication between NG2(+) Interstitial Cells and Myoblasts Promotes Muscle Growth in Neonates.
Specimen part
View SamplesDuring neonatal development, skeletal muscle grows dramatically by myonuclei accretion to existing fibers and hypertophic growth of fibers with protein synthesis. Overall design: To understand molecular mechanism underlying neonatal muscle growth, we used RNAseq to profile the global program of gene expressions especially involved in myoblast fusion, migration, and muscle fiber growth by itself. We used two biological replicates for each time point.
An NF-κB--EphrinA5-Dependent Communication between NG2(+) Interstitial Cells and Myoblasts Promotes Muscle Growth in Neonates.
Specimen part, Subject
View SamplesOligodendrocytes have recently been implicated in the pathophysiology of amyotrophic lateral sclerosis (ALS). Here we differentiated fibroblasts into induced neural progenitors and subsequently into oligodendrocytes and astrocytes. To confirm that the cells obtained with this protocol express the gene signature of oligodendrocytes, we performed a small gene expression study limited to four iOligodendrocyte lines from two controls (nos. 155 and 170) and two patients (nos. 12 and 17), four iAstrocyte lines from the same samples, and four fibroblast lines from one of our previously published studies
Oligodendrocytes contribute to motor neuron death in ALS via SOD1-dependent mechanism.
Specimen part, Disease
View SamplesAnalysis of the transcriptome of mononuclear side population (SP) and main population (MP) cells of human fetal skeletal muscle from 12 human subjects of gestational age 14-18 weeks.
Regulation of myogenic progenitor proliferation in human fetal skeletal muscle by BMP4 and its antagonist Gremlin.
Specimen part
View SamplesFunctional analysis of ABCB5 in A375 and G3361 melanoma cells, by comparing stably-transfected controls to ABCB5-shRNA-targeted cells.
ABCB5 maintains melanoma-initiating cells through a proinflammatory cytokine signaling circuit.
Specimen part, Cell line
View SamplesTo find BMAL1-regulated genes in mice pituitary gland we performed a differential microarray from wild-type vs Bmal1-/- knock-out mice
Chromatin remodeling as a mechanism for circadian prolactin transcription: rhythmic NONO and SFPQ recruitment to HLTF.
Sex, Specimen part
View SamplesGlucocorticoids remain the most widely used class of anti-inflammatory and immunosuppressive agents. They act primarily by binding to the glucocorticoid receptor, resulting in direct and indirect effects on gene expression. The current understanding of glucocorticoid effects on transcription in human cells is based mostly on studies of cancer cell lines, immortalized cell lines, or highly mixed populations of primary cells (such as peripheral blood mononuclear cells). To advance the understanding of the transcriptome-wide effects of glucocorticoids on highly pure populations of primary human cells, we performed RNA-seq on nine such cell populations at two time points after in vitro exposure to methylprednisolone or vehicle. Overall design: Nine cell types were studied: four hematopoietic (circulating B cells, CD4+ T cells, monocytes, and neutrophils) and five non-hematopoietic (endothelial cells, fibroblasts, myoblasts, osteoblasts, and preadipocytes). Each cell type was obtained from a separate cohort of 4 unrelated healthy human donors (4 biological replicates per cell type: BR1 - BR4). Cells form each donor were independently cultured and exposed in vitro to glucocorticoid or vehicle. Non-hematopoietic cells were incubated until the early plateau phase of growth, then exposed to methylprednisolone or vehicle. Hematopoietic cells were collected from peripheral blood, purified by magnetic selection (negative selection for B cells, CD4+ T cells and neutrophils; positive selection for monocytes). Purified B cells, CD4+ T cells, and monocytes were incubated overnight, then exposed to methylprednisolone or vehicle. Purified neutrophils were cultured for 4 hours, then exposed to methylprednisolone or vehicle. Ethanol was used as a vehicle for methylprednisolone. Estimated final concentrations were 8500 mcg/L (22.7 mcM) for methylprednisolone and 0.07% (15.57 mM) for ethanol (vehicle). For each cell type, samples were collected at two time points after treatment with methylprednisolone or vehicle: 2 hours and 6 hours. Samples were collected into TRIzol reagent and frozen at -80°C prior to RNA extraction. RNA-seq data for all samples is made available in this GEO Series.
Immune regulation by glucocorticoids can be linked to cell type-dependent transcriptional responses.
Specimen part, Subject, Time
View SamplesMelanoma growth is driven by malignant melanoma initiating cells (MMIC) identified by expression of the ATP-binding cassette (ABC) member, ABCB5. ABCB5+ melanoma subpopulations have been shown to overexpress the vasculogenic differentiation markers CD144 (VE-cadherin) and TIE-1 and are associated with CD31-negative vasculogenic mimicry (VM), an established biomarker associated with increased patient mortality. Here we identify a critical role for VEGFR-1 signaling in ABCB5+ MMIC-dependent VM and tumor growth. Global gene expression analyses, validated by mRNA and protein determinations, revealed preferential expression of VEGFR-1 on ABCB5+ tumor cells purified from clinical melanomas and established melanoma lines. In vitro, VEGF induced in a VEGFR-1-dependent manner expression of CD144 in ABCB5+ subpopulations that constitutively expressed VEGFR-1, but not in ABCB5- bulk populations that were predominantly VEGFR-1-negative. In vivo, melanomaspecific shRNA-mediated knockdown of VEGFR-1 blocked the development of ABCB5+ VM morphology and inhibited ABCB5+ VM-associated production of the secreted melanoma mitogen, laminin. Moreover, melanoma-specific VEGFR-1 knockdown markedly inhibited tumor growth (by >90%). Our results demonstrate that VEGFR-1 function in MMIC regulates VM and associated laminin production, and show that this function represents one mechanism through which MMIC promote tumor growth.
VEGFR-1 expressed by malignant melanoma-initiating cells is required for tumor growth.
Specimen part
View SamplesC1q suppresses JAK-STAT signal transduction and activates PPAR-mediated transcription in macrophages during clearance of modified forms of LDL leading to a reduction in inflammatory response. Overall design: Human monocyte-derived macrophages (HMDM) were incubated with either oxidized (oxLDL) or acetylated low-density lipoprotein (acLDL) in the presence or absence of C1q for 3 hours. Total RNA was extracted using the Qiagen RNeasy Mini Kit. RNA libraries were constructed using the Illumina TruSeq Stranded mRNA Sample Preparation Kit. Sequences were aligned to a reference genome (hg38), RPKM and raw counts were determined using CASAVA version 1.8.2.
Transcriptome data and gene ontology analysis in human macrophages ingesting modified lipoproteins in the presence or absence of complement protein C1q.
Specimen part, Subject
View SamplesNext generation sequencing of OPCs grown on stiff and soft hydrogels Overall design: Illumina HiSeq4000 PE150 Sequencing
Niche stiffness underlies the ageing of central nervous system progenitor cells.
Specimen part, Subject
View Samples