Angiotensin II (Ang II)-mediated vascular smooth muscle cells (VSMC) dysfunction plays a critical role in cardiovascular diseases. However, the gene expression in this process is unclear.
Small RNA sequencing reveals microRNAs that modulate angiotensin II effects in vascular smooth muscle cells.
Specimen part, Time
View SamplesAngiotensin II (Ang II)-mediated vascular smooth muscle cells (VSMC) dysfunction plays a critical role in cardiovascular diseases. However, the role of microRNAs (miRNAs) in this process is unclear. We used small RNA deep sequencing to profile Ang II-regulated miRNAs in rat VSMC and evaluated their role in VSMC dysfunction. Sequencing results revealed several Ang II-responsive miRNAs and bioinformatics analysis showed that their predicted targets can modulate biological processes relevant to cardiovascular diseases. Overall design: Examined 4 samples of Rat VSMC. Control (without Ang II treatment) and 3 samples treated with Ang II for 1h, 3h, and 24h. Compared the changes in gene expression in Ang II treated samples relative to control samples.
Small RNA sequencing reveals microRNAs that modulate angiotensin II effects in vascular smooth muscle cells.
No sample metadata fields
View SamplesThe LXR-regulated E3 ubiquitin ligase IDOL controls LDLR receptor stability independent of SREBP and PCSK9, but its relevance to plasma lipid levels is unknown. Here we demonstrate that the effects of the LXRIDOL axis are both tissue- and species-specific. In mice, LXR agonist induces Idol expression in peripheral tissues but not in liver, and does not change plasma LDL levels. Accordingly, Idol-deficient mice exhibit elevated LDLR protein levels in peripheral tissues but not in the liver and have minimal change in plasma LDL levels. By contrast, LXR activation in cynomolgus monkeys induces hepatic IDOL expression, reduces LDLR protein, and raises plasma LDL levels. Knockdown of IDOL in monkeys with an antisense oligonucleotide blunts the effect of LXR agonist on LDL levels. These results implicate IDOL as a modulator of plasma lipid levels in primates and support further investigation into IDOL inhibition as a strategy for LDL lowering in humans.
The LXR-Idol axis differentially regulates plasma LDL levels in primates and mice.
Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A formalin-fixed paraffin-embedded (FFPE)-based prognostic signature to predict metastasis in clinically low risk stage I/II microsatellite stable colorectal cancer.
Sex, Age
View SamplesThis study was conducted in order to identify biomarkers for a prognostic gene expression signature for metastases in early stage CRC.
A formalin-fixed paraffin-embedded (FFPE)-based prognostic signature to predict metastasis in clinically low risk stage I/II microsatellite stable colorectal cancer.
Sex, Age
View SamplesTranscriptome analysis of RNAs extracted from 2 hour-TGF-b-treated or untreated LX-2 cells with or without STAT3 knockdown
Transforming Growth Factor-β (TGF-β) Directly Activates the JAK1-STAT3 Axis to Induce Hepatic Fibrosis in Coordination with the SMAD Pathway.
Treatment, Time
View SamplesTranscriptome analysis of RNAs extracted from livers of wild type or Smurf1 knock out (KO) or Smurf2 KO mice at age of 11 month old.
Non-proteolytic ubiquitin modification of PPARγ by Smurf1 protects the liver from steatosis.
Age, Specimen part
View SamplesThe pulmonary alveolar epithelium which play key role in lung biological function is mainly composed of two types of epithelial cells: alveolar type I (AT1) and type II (AT2) cells. We know very little about developmental heterogeneity of the AT1 cell population. By using 10X genomics “Chromium Single Cell” technology, we performed single-cell RNA-seq (scRNA-seq) analyses of AT1 cells at postnatal day 3 (P3), P15, and P60, along with AT2 cells (P60) in mice. Our study identified a robust new genetic marker (Igfbp2) of postnatal AT1 cells. The study also provided the transcriptome information of AT1 cells during alveologensis. Overall design: We performed 10X genomics single-cell RNA-seq at various developmental stages of AT1 cells of lungs at postnatal (P)3, P15, and P60. We also performed 10X genomics single-cell RNA-seq of AT2 cells of P60 lungs.
Pulmonary alveolar type I cell population consists of two distinct subtypes that differ in cell fate.
Specimen part, Cell line, Subject
View SamplesEnhanced secondary Ab responses are a vital component of adaptive immunity, yet little is understood about the intrinsic and extrinsic regulators of nave and memory B cells that results in differences in their responses to Ag. Microarray analysis, together with surface and intracellular phenotyping, revealed that memory B cells have increased expression of members of the TNF receptor, SLAM, B7 and Bcl2 families, as well as the TLR-related molecule CD180 (RP105). Accordingly, memory B cells exhibited enhanced survival, proliferation and Ig secretion, as well as entered division more rapidly than nave B cells in response to both T-dependent and T-independent stimuli. Furthermore, both IgM and isotype switched memory B cells, but not nave B cells, co-stimulated CD4+ T cells in vitro through a mechanism dependent on their constitutive expression of CD80 and CD86. This study demonstrates that upregulation of genes involved in activation, co-stimulation and survival provides memory B cells with a unique ability to produce enhanced immune responses and contributes to the maintenance of the memory B cell pool.
Resting human memory B cells are intrinsically programmed for enhanced survival and responsiveness to diverse stimuli compared to naive B cells.
Specimen part
View SamplesMECP2 duplication syndrome, a childhood neurological disorder characterized by autism, intellectual disability, motor dysfunction, anxiety and epilepsy, is caused by a duplication on chromosome Xq28 spanning the MECP2 gene that results in doubling of MeCP2 levels. MECP2 overexpression in mice causes neurobehavioral and electroencephalographic defects similar to those of human patients, but the gross anatomy of the brain remains unaffected. We hypothesized that MECP2 duplication syndrome would be reversible and tested two methods to restore MeCP2 levels to normal: conditional genetic recombination and antisense oligonucleotide therapy. Both approaches rescued molecular, physiological and behavioral features of adult symptomatic mice. Antisense therapy also restored normal MeCP2 levels in lymphoblastoid cells from MECP2 duplication patients, in a dose-dependent manner. Our data indicate that antisense oligonucleotides could provide a viable therapeutic approach for human MECP2 duplication syndrome as well as other disorders involving copy number gains. Overall design: Hippocampal mRNA profiles of conditional MECP2 overexpression and genetic rescue mice were generated by deep sequencing, in triplicate, using Illumina TruSeq.
Reversal of phenotypes in MECP2 duplication mice using genetic rescue or antisense oligonucleotides.
No sample metadata fields
View Samples