MicroRNAs expression in 20(R)-ginsenoside Rg3-induced anti-angiogenesis
Ontology highlight
ABSTRACT: The angio-suppressive effect of 20(R)-ginsenoside Rg3 (Rg3-R) has been previously demonstrated, and microRNAs (miRNAs) are a vital group of small non-coding RNAs that function as post-transcriptional modulator of gene expression. Thus, using human umbilical vein endothelial cells (HUVEC) as model, we compared the microRNA (miRNA) expression profile of vascular endothelial growth factor (VEGF)-induced cells with the profile of the cell co-treated with VEGF and Rg3-R. Among the screened 553 human miRNAs, 6 up-regulated (miR-520h, miR-487b, miR-197, miR-524*, miR-342 and miR-219) and 3 down-regulated (miR-23a, miR-489 and miR-377) miRNAs were detected in Rg3-R treated vascular endothelial growth factor (VEGF)-induced HUVECs compared to VEGF alone. Real time RT-PCR was subsequently performed to verify the miRNA microarray result. Two condition experiment: VEGF-induced HUVEC and VEGF-induced HUVEC treated with Rg3-R. Three independent microarray experiments, with triplicate per microarray.
Project description:MicroRNAs (miRNAs) are small non-coding RNAs that act as post-transcriptional gene modulators. Ginsenoside-Rg1, one of the active components of ginseng, has been confirmed by us as an angiogenesis inducer. Using miRNA microarray analysis, a total of 15 (including miR-214) and 3 miRNAs were found to be down- or up-regulated by Rg1 in human umbilical vein endothelial cells (HUVEC), respectively. Since miR-214 is closely related to endothelial nitric oxide synthase (eNOS) and hence angiogenesis; its expression was further validated by qRT-PCR. We also investigated the role of miR-214 on eNOS expression and in tubulogenesis of HUVEC by transfection of specific miRNA inhibitor or precursor. Our results suggested that Rg1 can down-regulate miR-214 expression in HUVEC, leading to an increase in eNOS expression which can promote angiogenesis. This result signifies a new understanding towards how a simple natural compound can affect physiological changes through modulation of miRNA expression. The study is used to investigate the role of miRNA-214 in Rg1-induced human endothelial cells.
Project description:This study investigates the regional expression profiles of microRNAs (miRNAs) in endothelial cells isolated from the athero-protective descending thoracic aorta (DT) and from the athero-susceptible aortic arch (AA) in a swine model. Seven 2-channel assays comparing DT samples to AA samples were performed using the Invitrogen NCode Multi-Species miRNA Microarray.
Project description:Proteomic analysis of differentially expressed proteins in MDA-MB-231 and MCF-10A cell lines when miR-200c and miR-203 were transiently expressed or inhibited, respectively.
Project description:We examined hypoxia responsing miRNAs in HUVEC and MA148cells. Microarray studies revealed hypoxia can change microRNA expression in HUVEC and MA148 cells. 8 HUVEC samples (4 controls and 4 experimentals) and 4 MA148 samples (2 controls and 2 experimentals)
Project description:The angio-suppressive effect of 20(R)-ginsenoside Rg3 (Rg3-R) has been previously demonstrated, and microRNAs (miRNAs) are a vital group of small non-coding RNAs that function as post-transcriptional modulator of gene expression. Thus, using human umbilical vein endothelial cells (HUVEC) as model, we compared the microRNA (miRNA) expression profile of vascular endothelial growth factor (VEGF)-induced cells with the profile of the cell co-treated with VEGF and Rg3-R. Among the screened 553 human miRNAs, 6 up-regulated (miR-520h, miR-487b, miR-197, miR-524*, miR-342 and miR-219) and 3 down-regulated (miR-23a, miR-489 and miR-377) miRNAs were detected in Rg3-R treated vascular endothelial growth factor (VEGF)-induced HUVECs compared to VEGF alone. Real time RT-PCR was subsequently performed to verify the miRNA microarray result.
Project description:Our analyses of microRNA expression profiles involve the hybridization of fluorescently labeled miRNA samples to custom made, DNA microarrays based on the GAPSII coated slides. We hybridized different amounts of microRNAs from the mirVana miRNA Reference Panel v9.1 to microarrays. Keywords: Expression Three different concentrations of miRNAs from the commercial standrads were labelled and hybridized to three microarrays.
Project description:This SuperSeries is composed of the following subset Series: GSE17058: MiRNA expression in adipose tissue and liver from a spontaneous rat model of Type 2 diabetes GSE17059: Gene expression in adipose tissue and liver from a spontaneous rat model of Type 2 diabetes Refer to individual Series
Project description:MicroRNAs (miRNAs) are non-coding RNA molecules involved in post-transcriptional control of gene expression of a wide number of genes, including those involved in glucose homeostasis. Type 2 diabetes (T2D) is characterized by hyperglycaemia and defects in insulin secretion and action at target tissues. Using a miRNA microarray platform, we sought to establish differences in miRNA expression in two insulin-target tissues (liver and adipose tissue) from seven-month-old spontaneously diabetic (Goto-Kakizaki [GK]) and non-diabetic (Brown-Norway [BN]) rats. MiRNA data were integrated with gene expression data from the same rats to investigate how differentially expressed miRNAs affected the expression of their predicted target genes. Two-colour experiment comparing GK and BN rat strains for two different tissues. Biological replicates: 4 GK and 4 BN rats; adipose tissue and liver extracted from each rat. Two samples were hybridised to each array (one of each strain, same tissue)
Project description:MicroRNAs (miRNAs) play an important role in human brain development and maintenance. To search for miRNAs potentially involved with molecular mechanisms in the pathogenesis of Parkinsons disease (PD), we utilized miRNA microarrays to identify expression changes of 115 annotated Caenorhabditis elegans (C.elegans) miRNAs in human α-synuclein A53T transgenic, dopamine deficient catecholamine transporter gene cat-1 mutant and parkin gene pdr-1 mutant C.elegans strains. Twelve miRNAs were found regulated differentially in α-synuclein transgenic C. elegans, five in cat-1 mutants and three in pdr-1 mutants. The family of miR64/65 appeared co-under-expressed in α-synuclein and cat-1 strains and members of let-7 family co-under-expressed (except miR-241 over-expressed) in a-synuclein and pdr-1 strains. Class H serpentine receptor (srh) family of G-protein-coupled receptor genes were computationally identified to be highly over-represented target candidates for regulated miRNAs.These results indicate that miRNAs are misregulated in C. elegans PD models and suggest a role for these molecules in the disease pathogenesis. Two color NCode microRNA microrarrays were used (Invitrogen) to measure miRNA expression changes in human alpha-synuclein trangenic, cat-1 mutant, and pdr-1 mutant C.elegans strains. The experiment contains four independent biological replicates (worm populations)/strain. Strain N2 was used as reference channel, also prepared from four independently isolated small RNA samples.
Project description:Defects in stress responses are important contributors in many chronic conditions including cancer, cardiovascular disease, diabetes, and obesity-driven pathologies like non-alcoholic steatohepatitis (NASH). Specifically, endoplasmic reticulum (ER) stress is linked with these pathologies and control of ER stress can ameliorate tissue damage. MicroRNAs have a critical role in regulating diverse stress responses including ER stress. Here we show that miR-494-3p plays a functional role during ER stress. ER stress inducers (tunicamycin and thapsigargin) robustly increase the expression of miR-494 in vitro in an ATF6 dependent manner. Surprisingly, miR-494 pretreatment dampens the induction and magnitude of ER stress in response to tunicamycin in endothelial cells. Conversely, inhibition of miR-494 increases ER stress de novo and amplifies the effects of ER stress inducers. Using Mass Spectrometry (TMT-MS) we identified many proteins that are downregulated by both tunicamycin and miR-494 in cultured human umbilical vein endothelial cells (HUVECs). Among these, we found 6 transcripts which harbor a putative miR-494 binding site. Our data indicates that ER stress driven miR-494 may act in a feedback inhibitory loop to dampen downstream ER stress signaling. We propose that RNA-based approaches targeting miR-494 or its targets may be attractive candidates for inhibiting ER stress dependent pathologies in human disease.