MiRNA in HUVEC culture supernatant
Ontology highlight
ABSTRACT:
ORGANISM(S): synthetic construct Homo sapiens
PROVIDER: GSE207436 | GEO | 2022/07/05
REPOSITORIES: GEO
Similar Datasets
Project description:Asymmetric dimethylarginine (ADMA) is a naturally occurring inhibitor of nitric oxide synthesis that accumulates in wide range of diseases associated with endothelial dysfunction and enhanced atherosclerosis. Plasma ADMA has been implicated as a major novel cardiovascular risk factor, but the mechanisms by which low concentrations of ADMA produce adverse effects on the cardiovascular system are unclear. We have treated human coronary artery endothelial cells with ADMA at 2uM (a pathophysiological dose) and 100uM (a pharmacological dose), for 24h.
2005-09-01 | E-MEXP-377 | biostudies-arrayexpress
Project description:Here we optimize the HCD Normalized Collision Energy (NCE) in order to generate neutral losses of monomethylamine and dimethylamine which can be lost by symmetric dimethylarginine and asymmetric dimethylarginine, respectively. By testing a range of NCEs across two different methyl enrichment techniques, we identified the optimal NCE as 32 to both generate neutral losses and to improve identifications of dimethyl PSMs. We achieve a 2-to-3 fold increase in the number of unique DMA peptides assigned neutral losses desginating them as ADMA or SDMA. This method will be useful to others interested in analyzing dimethylarginine peptides through mass spectrometry, where ADMA and SDMA have identical masses but differing neutral losses, and differing biological functions.
2020-05-27 | PXD017193 | Pride
Project description:miRNA in HUVEC culture supernatant
| PRJNA855475 | ENA
Project description:Levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, are increased in lung, sputum, exhaled breath condensate and plasma samples from asthma patients. ADMA is metabolized primarily by dimethylarginine dimethylaminohydrolase 1 (DDAH1) and DDAH2. We determined the effect of DDAH1 overexpression on development of allergic inflammation in mouse models of asthma. Wild type and DDAH1-transgenic mice were challenged with PBS or house dust mite (HDM). Airway inflammation was assessed by bronchoalveolar lavage (BAL) total and differential cell counts. Gene expression in lungs was determined by RNA-Seq and RT-quantitative PCR (qPCR). The expression of DDAH1 and DDAH2 was decreased in the lungs of mice following HDM exposure. Transgenic overexpression of DDAH1 resulted in decreased BAL total cell and eosinophil numbers following HDM exposure. Total IgE levels in serum and BAL fluid were decreased in HDM-exposed DDAH1-transgenic mice compared to HDM-exposed wild type mice. RNA-Seq results showed downregulation of genes in inducible nitric oxide synthase (iNOS) signaling pathway in PBS-treated DDAH1 transgenic mice versus PBS-treated wild type mice and downregulation of genes in IL-13/FOXA2 signaling pathway in HDM-treated DDAH1 transgenic mice versus HDM-treated wild type mice. Our findings suggest that decreased expression of DDAH1 in airway epithelial cells may contribute to allergic asthma and overexpression of DDAH1 attenuates allergen-induced airway inflammation through modulation of Th2 responses. mRNA profiles of WT and DDAH1-transgenic mice treated with PBS or house dust mite (HDM).
2013-12-03 | E-GEOD-49047 | biostudies-arrayexpress
Project description:<p>Mechanical force is critical for the development and remodeling of bone. Here we report that mechanical force regulates the production of the metabolite asymmetric dimethylarginine (ADMA) via regulating the hydrolytic enzyme dimethylarginine dimethylaminohydrolase 1 (Ddah1) expression in osteoblasts. The presence of -394 4N del/ins polymorphism of Ddah1 and higher serum ADMA concentration are negatively associated with bone mineral density. Global or osteoblast-specific deletion of Ddah1 leads to increased ADMA level but reduced bone formation. Further molecular study unveils that mechanical stimulation enhances TAZ/SMAD4-induced Ddah1 transcription. Deletion of Ddah1 in osteoblast-lineage cells fails to respond to mechanical stimulus-associated bone formation. Taken together, the study reveals mechanical force is capable of down-regulating ADMA to enhance bone formation.</p>
2021-11-23 | MTBLS3725 | MetaboLights
Project description:Levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, are increased in lung, sputum, exhaled breath condensate and plasma samples from asthma patients. ADMA is metabolized primarily by dimethylarginine dimethylaminohydrolase 1 (DDAH1) and DDAH2. We determined the effect of DDAH1 overexpression on development of allergic inflammation in a mouse model of asthma. The expression of DDAH1 and DDAH2 in mouse lungs was determined by RT-quantitative PCR (qPCR). ADMA levels in bronchoalveolar lavage fluid (BALF) and serum samples were determined by mass spectrometry. Wild type and DDAH1-transgenic mice were intratracheally challenged with PBS or house dust mite (HDM). Airway inflammation was assessed by bronchoalveolar lavage (BAL) total and differential cell counts. The levels of IgE and IgG1 in BALF and serum samples were determined by ELISA. Gene expression in lungs was determined by RNA-Seq and RT-qPCR. Our data showed that the expression of DDAH1 and DDAH2 was decreased in the lungs of mice following HDM exposure, which correlated with increased ADMA levels in BALF and serum. Transgenic overexpression of DDAH1 resulted in decreased BAL total cell and eosinophil numbers following HDM exposure. Total IgE levels in BALF and serum were decreased in HDM-exposed DDAH1-transgenic mice compared to HDM-exposed wild type mice. RNA-Seq results showed downregulation of genes in the inducible nitric oxide synthase (iNOS) signaling pathway in PBS-treated DDAH1-transgenic mice versus PBS-treated wild type mice and downregulation of genes in IL-13/FOXA2 signaling pathway in HDM-treated DDAH1-transgenic mice versus HDM-treated wild type mice. Our findings suggest that decreased expression of DDAH1 and DDAH2 in the lungs may contribute to allergic asthma and overexpression of DDAH1 attenuates allergen-induced airway inflammation through modulation of Th2 responses.
2013-12-03 | GSE49047 | GEO
Project description:Expression data of LoVo cells treated by 10μM asymmetric dimethylarginine (ADMA) for 96h in serum starvation medium
| PRJNA290040 | ENA
Project description:The roles of protein arginine methylation in the pathongenesis of chronic pancreatitis still remains poorly understood. In this study, we performed a proteomic identification of ADMA (asymmetric dimethylarginine)-containing proteins in clinical tissues collected from chronic pancreatitis patients using affinity purification combined with LC-MS/MS.
2021-05-20 | PXD026106 | iProX
Project description:Protein arginine methylation has been established an essential protein modification regulating cancer initiation and progression, but its implications in PDAC (Pancreatic ductal adenocarcinoma) still remains poorly elucidated. In this study, we characterized ADMA (asymmetric dimethylarginine)-bearing peptides in human pancreatic ductal epithelium cell line HPDE6c7 and PDAC cell line PANC-1 by a label-free quantitative proteomics combined with affinity purification.
2020-02-18 | PXD017577 | iProX
Project description:Question Addresses: What is the gene expression profile from human umbilical vein endothelial cells (HUVEC) and human Jurkat T cells after irradiation (IR)? What, if any, is the effect of co-culturing these two cell types on gene expression? There are eight experimental conditions for this experiment: (1) non-irradiated HUVEC; (2) irradiated HUVEC; (3) non-irradiated Jurkat; (4) irradiated Jurkat; (5) non-irradiated HUVEC + non-irradiated Jurkat+; (6) non-irradiated HUVEC + irradiated Jurkat; (7) irradiated HUVEC + non-irradiated Jurkat; (8) irradiated HUVEC + irradiated Jurkat. A common, pooled reference consisting of RNA taken from conditions 1-8 as described above was used for all hybridizations.
2022-06-03 | GSE39019 | GEO