In the current study we sought to investigate systemic effects of aneurysmal subarachnoid hemorrhage (SAH) through analysis of gene expression profiles in peripheral blood cells by means of deep transcriptome sequencing. We included 19 patients in the acute phase of IA rupture (RAA, first 72 hours), 20 patients in the chronic phase (RAC, 3-15 months), and 20 controls. We performed a global analysis of protein coding and non-coding gene variants regulated by SAH. We investigated expression of specific gene variants that may lead to production of functionally distinct protein isoforms and influence systemic response to IA rupture.
No associated publication
Sex, Age, Specimen part, Disease
View SamplesUmkirch-1/Umkirch-3 hybrid plants and their parents were grown at 23SD and then shifted to 16SD for five days. 10 plants were pooled in each of three sample replicates.
Autoimmune response as a mechanism for a Dobzhansky-Muller-type incompatibility syndrome in plants.
Specimen part
View SamplesRNASeq time course (1,2,3 hrs) of Pseudomonas aeruginosa (UCBPP-PA14) on plastic (polystyrene) petri dish
No associated publication
Specimen part, Disease, Cell line
View SamplesAssessing the impact of HIV-1 infection on trancriptional program of quiescent CD4 T lymphocytes. Such cells were made susceptible to HIV-1 by dowmodulating SAMHD1 restriction factor using VLP-Vpx without any activation signal.
CD32a is a marker of a CD4 T-cell HIV reservoir harbouring replication-competent proviruses.
Sex, Specimen part
View SamplesCritically ill, immobilized and mechanically ventilated intensive care unit (ICU) patients develop severe muscle wasting and impaired muscle function. This condition is referred to as critical illness myopathy (CIM). This study aimed to obtain the gene signature of CIM. Percutaneous conchotome muscle biopsies from the tibialis anterior muscle was used for RNA sequencing from seven mechanically ventilated ICU patients and six control subjects.
No associated publication
Sex, Age, Specimen part
View SamplesThere is increasing interest in using primary nasal epithelial cells (PNECs) instead of primary bronchial epithelial cells (PBECs) in order to study epithelial responses in rhinitis and asthma. This study aimed to establish a robust cell culture model appropriate for studying rhinovirus infection and the consequent epithelial responses in asthma and rhinitis. First, a comprehensive comparison of fresh and cryopreserved primary nasal epithelial cells from three donors before and after RV infection was conducted, using high throughput RNA sequencing and transcriptomics.
No associated publication
Sex, Age, Specimen part
View SamplesGenomic instability promotes evolution and heterogeneity of tumors. Unraveling its mechanistic basis is essential to design appropriate therapeutic strategies. In a recent study we reported an unexpected oncogenic property of p21WAF1/Cip1 showing that its chronic expression, in a p53-deficient environment, causes genomic instability by deregulating the replication licensing machinery.
No associated publication
Sex, Specimen part
View SamplesSmall RNA seq following over expression of miR-218 in HepG2 cells; mRNA expression following perturbation of miR-218 in primary mouse motor neurons
No associated publication
Sex, Specimen part
View SamplesRNA-seq data for cell lines in the haematopoietic lineages, hematological malignancy
No associated publication
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View SamplesClass IIa histone deacetylases (HDACs) are signal-responsive regulators of gene expression involved in vascular homeostasis. To investigate the differential role of class IIa HDACs for the regulation of angiogenesis, we used siRNA to specifically suppress the individual HDAC isoenzymes. Among the HDAC isoforms tested, silencing of HDAC5 exhibited a unique pro-angiogenic effect evidenced by increased endothelial cell migration, sprouting and tube formation. Consistently, overexpression of HDAC5 decreased sprout formation, indicating that HDAC5 is a negative regulator of angiogenesis. The anti-angiogenic activity of HDAC5 was independent of MEF2 binding and its deacetylase activity, but required a nuclear localization indicating that HDAC5 might affect the transcriptional regulation of gene expression. To identify putative HDAC5 targets, we performed microarray expression analysis. Silencing of HDAC5 increased the expression of fibroblast growth factor 2 (FGF2) and angiogenic guidance factors including Slit2. Antagonization of FGF2 or Slit2 reduced sprout induction in response to HDAC5 siRNA. ChIP assays demonstrate that HDAC5 binds to the promoter of FGF2 and Slit2. In summary, HDAC5 represses angiogenic genes, like FGF2 and Slit2, which causally contribute to capillary-like sprouting of endothelial cells. The de-repression of angiogenic genes by HDAC5 inactivation may provide a useful therapeutic target for induction of angiogenesis.
HDAC5 is a repressor of angiogenesis and determines the angiogenic gene expression pattern of endothelial cells.
Specimen part
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