To 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 SamplesS. epidermidis ability to form biofilms on indwelling medical devices and its association with the emergence of chronic infections is its main virulence factor. Nevertheless, it has been shown that the cells released from these biofilms are associated with the advent of serious acute infections with bacteraemia as one of the major clinical manifestations. Despite their clinical relevance, very little is known about the impact of biofilm-released cells in pathogenesis. Hence, herein, we characterized the murine immune response to the presence of cells released from S. epidermidis biofilms analysing spleen cells transcriptome by microarrays. These findings may help to explain the recurrent inflammatory symptoms presented by patients with colonization of indwelling medical devices.
<i>Staphylococcus epidermidis</i> Biofilm-Released Cells Induce a Prompt and More Marked <i>In vivo</i> Inflammatory-Type Response than Planktonic or Biofilm Cells.
Sex, Specimen part
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 SamplesFsh-mediated regulation of zebrafish spermatogenesis includes modulating the expression of testicular growth factors. Here, we study if and how two Sertoli cell-derived Fsh-responsive growth factors, anti-Müllerian hormone (Amh; inhibiting steroidogenesis and germ cell differentiation) and insulin-like growth factor 3 (Igf3; stimulating germ cell differentiation), cooperate in regulating spermatogonial development. In dose response and time course experiments with primary testis tissue cultures, Fsh upregulated igf3 transcript levels and down-regulated amh transcript levels; igf3 transcript levels were more rapidly up-regulated and responded to lower Fsh concentrations than were required to decrease amh mRNA levels. Quantification of immunoreactive Amh and Igf3 on testis sections showed that Fsh increased slightly Igf3 staining but decreased clearly Amh staining. Studying the direct interaction of the two growth factors showed that Amh compromised Igf3-stimulated proliferation of type A (both undifferentiated [Aund] and differentiating [Adiff]) spermatogonia. Also the proliferation of those Sertoli cells associated with Aund spermatogonia was reduced by Amh. To gain more insight into how Amh inhibits germ cell development, we examined Amh-induced changes in testicular gene expression by RNA sequencing. The majority (69%) of the differentially expressed genes was down-regulated by Amh, including several stimulators of spermatogenesis, such as igf3 and steroidogenesis-related genes. At the same time, Amh increased the expression of inhibitory signals, such as inha and id3, or facilitated prostaglandin E2 (PGE2) signaling. Evaluating one of the potentially inhibitory signals, we indeed found in tissue culture experiments that PGE2 promoted the accumulation of Aund at the expense of Adiff and B spermatogonia. Our data suggest that an important aspect of Fsh bioactivity in stimulating spermatogenesis is implemented by restricting the different inhibitory effects of Amh and by counterbalancing them with stimulatory signals, such as Igf3 Overall design: 10 samples in total were analyzed: 5 biological replicates from control testis samples and 5 biological replicates from Amh-treated testis samples (all co-incubated with 11KT)
Antagonistic regulation of spermatogonial differentiation in zebrafish (Danio rerio) by Igf3 and Amh.
No sample metadata fields
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 SamplesEndocardial (EE) and Aortic (AE) endothelial cells were isolated from the same two rats, pooled (EE and AE kept separately) and cultured for 2 passages. Culture conditions and confluence of EE and AE cell cultures were kept as identical as possible. RNA was isolated and the expression profile of both endothelial cell types was compared using the Affymetrix rat genome U34A array.
Molecular diversity of cardiac endothelial cells in vitro and in vivo.
No sample metadata fields
View SamplesIn addition to the recently published in situ transcriptomics of LCL skin lesions (Novais et al., Khouri et al.), we herein present the first systemic disease signature of localized cutaneous leishmaniasis (LCL), using Affymetrix microarrays (HuGene 1.0) followed by systems biology analysis of the PBMC transciptome of LCL patients (n=18), as compared to healthy controls (n=12).
Systems Approach Reveals Nuclear Factor Erythroid 2-Related Factor 2/Protein Kinase R Crosstalk in Human Cutaneous Leishmaniasis.
Specimen part, Disease stage
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 SamplesThe purpose of this experiment was to identify genes responding differently to a 24 h low red to far red ratio (R:FR) treatment in plants grown at 16 and 22 degrees
Light-quality regulation of freezing tolerance in Arabidopsis thaliana.
Age
View Samples