Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27600600_1.fastq.gz | Fastqsanger.gz | |||
| SRR27600600_2.fastq.gz | Fastqsanger.gz | |||
| SRR27600601_1.fastq.gz | Fastqsanger.gz | |||
| SRR27600601_2.fastq.gz | Fastqsanger.gz | |||
| SRR27600602_1.fastq.gz | Fastqsanger.gz |
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Project description:The mechanism by which aging induces aortic aneurysm and dissection (AAD) remains unclear. A total of 430 subjects were recruited for screening of differentially expressed plasma microRNAs. We found that miR-1204 was significantly increased in both plasma and aorta of elder patients with AAD, and was positively correlated with age. Cell senescence induced the expression of miR-1204 through p53 interaction with plasmacytoma variant translocation 1, and miR-1204 induced vascular smooth muscle cell (VSMC) senescence to form a positive feedback loop. miR-1204 aggravated angiotensin II-induced AAD formation, and inhibition of miR-1204 attenuated β-aminopropionitrile monofumarate-induced AAD formation. Mechanistically, miR-1204 directly targeted myosin light chain kinase (MYLK) to promote VSMCs to acquire senescence-associated secretory phenotype (SASP) and lose their contractile phenotype. Overexpression of MYLK reversed miR-1204-induced VSMC senescence, SASP and contractile phenotype changes, and the decrease of transforming growth factor-β signaling pathway. Our findings suggest aging aggravates AAD via 75 miR-1204-MYLK signaling axis.
2024-04-02 | GSE253747 | GEO
Project description:The mechanism by which aging induces aortic aneurysm and dissection (AAD) remains unclear. We found that miR-1204 was significantly increased in both plasma and aorta of elder patients with AAD, and was positively correlated with age. Cell senescence induced the expression of miR-1204 through p53 interaction with plasmacytoma variant translocation 1, and miR-1204 induced vascular smooth muscle cell (VSMC) senescence to form a positive feedback loop.
2024-04-02 | GSE255157 | GEO
Project description:Acute aortic dissection (AAD) is one of the major aortic diseases that occurs without a preceding symptom and often results in sudden death. Despite the recent advances in cardiovascular medicine, AAD remains a serious problem because its molecular pathogenesis is largely unknown. In this paper, we report our serendipitous discovery that stress-induced expression of tenascin C (TNC), a member of matricellular proteins, is the protection mechanism of aorta to prevent AAD. The aortic wall stress imposed by the aortic stiffening and the angiotensin II infusion caused the strong induction of TNC in wild type mouse aorta without gross morphological changes. While TNC knockout mice at the baseline showed no morphological, histological or biomechanical abnormalities of aorta, deletion of TNC gene rendered the aorta susceptible to AAD upon the aortic stress. The stressed TNC-null aorta showed the loss of the tensile strength due to the insufficient expression of extracellular matrix proteins and the exaggerated proinflammatory response before the onset of AAD. Therefore, TNC works as a stress-activated molecular damper both by reinforcing the tensile strength and by limiting the excessive proinflammatory response in aorta. Thus far, the molecular event that leads to the AAD development has been unclear because of the unpredictable nature of the AAD onset. This study sheds light on the previously unrecognized tissue protection mechanism that converts the potentially harmful stress response into the active reinforcement of the aorta, of which failure leads to the development of AAD. Although TNC is expressed in various tissues upon the mechanical and proinflammatory stimuli, its role has long been a mystery. Our data uncovered the adaptive role of TNC in aorta that must be resilient to the continuous hemodynamic and humoral stress for lifetime.
2015-03-27 | GSE36899 | GEO
Project description:The mechanism by which aging induces aortic aneurysm and dissection (AAD) remains unclear. A total of 430 subjects were recruited for screening of differentially expressed plasma microRNAs. We found that miR-1204 was significantly increased in both plasma and aorta of elder patients with AAD, and was positively correlated with age. Cell senescence induced the expression of miR-1204 through p53 interaction with plasmacytoma variant translocation 1, and miR-1204 induced vascular smooth muscle cell (VSMC) senescence to form a positive feedback loop. miR-1204 aggravated angiotensin II-induced AAD formation, and inhibition of miR-1204 attenuated β-aminopropionitrile monofumarate-induced AAD formation. Mechanistically, miR-1204 directly targeted myosin light chain kinase (MYLK) to promote VSMCs to acquire senescence-associated secretory phenotype (SASP) and lose their contractile phenotype. Overexpression of MYLK reversed miR-1204-induced VSMC senescence, SASP and contractile phenotype changes, and the decrease of transforming growth factor-β signaling pathway. Our findings suggest aging aggravates AAD via miR-1204-MYLK signaling axis.
2024-04-01 | PXD048658 | Pride
Project description:Acute aortic dissection (AAD) is one of the major aortic diseases that occurs without a preceding symptom and often results in sudden death. Despite the recent advances in cardiovascular medicine, AAD remains a serious problem because its molecular pathogenesis is largely unknown. In this paper, we report our serendipitous discovery that stress-induced expression of tenascin C (TNC), a member of matricellular proteins, is the protection mechanism of aorta to prevent AAD. The aortic wall stress imposed by the aortic stiffening and the angiotensin II infusion caused the strong induction of TNC in wild type mouse aorta without gross morphological changes. While TNC knockout mice at the baseline showed no morphological, histological or biomechanical abnormalities of aorta, deletion of TNC gene rendered the aorta susceptible to AAD upon the aortic stress. The stressed TNC-null aorta showed the loss of the tensile strength due to the insufficient expression of extracellular matrix proteins and the exaggerated proinflammatory response before the onset of AAD. Therefore, TNC works as a stress-activated molecular damper both by reinforcing the tensile strength and by limiting the excessive proinflammatory response in aorta. Thus far, the molecular event that leads to the AAD development has been unclear because of the unpredictable nature of the AAD onset. This study sheds light on the previously unrecognized tissue protection mechanism that converts the potentially harmful stress response into the active reinforcement of the aorta, of which failure leads to the development of AAD. Although TNC is expressed in various tissues upon the mechanical and proinflammatory stimuli, its role has long been a mystery. Our data uncovered the adaptive role of TNC in aorta that must be resilient to the continuous hemodynamic and humoral stress for lifetime. We used periaortic application of 0.5 M CaCl2 to the infrarenal aorta or either wild type (WT) or tenascin C knockout (TNC-KO) mice to create the mouse model for stiffened aorta and infused the mice with AngII (1 µg/min/kg) for 1 week to apply the pathological stress on aorta (Ca+AngII). Mice were then killed with an overdose of pentobarbital to obtain the tissue samples. The suprarenal aortic samples, from the level of right renal artery to 10 mm above the right renal artery, and infrarenal aortic samples, from the level of left renal artery to 10 mm below the left renal artery, were collected and kept in RNAlater (Qiagen) until the extraction of total RNA using RNeasy (Qiagen). We obtained the RNA samples from 8 mice with Ca+AngII treatment and 5 mice without Ca+AngII treatment for each genotype. We pooled the RNA samples with the identical experimental condition to perform the transcriptome analysis using Mouse Genome 430 2.0 (Affymetrix). We obtained suprarenal aortic smooth muscle cells (ASMCs) from TNC-KO mice by enzymatic dispersion and cultured them in Dulbecco's modified Eagle medium (DMEM) supplemented with 10% fetal bovine serum. We cultured TNC-KO ASMCs in the presence or absence of exogenous TNC (10 µg/mL) and stimulated the cells with 10 ng/mL TNF-alpha for 24 h before obtaining total RNA using RNeasy. We used 3 independent ASMC cultures without the exogenous TNC and 4 independent cultures with the exogenous TNC. We hybridized each of the RNA samples individually to Mouse Genome 430 2.0 Array (Affymetrix).
2015-03-27 | E-GEOD-36899 | biostudies-arrayexpress
Project description:The estimation of the post-mortem interval (PMI) and the age-at-death (AAD) are crucial steps in the medico-legal investigation of unidentified human remains. Current methods to estimate PMI and AAD suffer from a lack of accuracy and objectivity, particularly when the remains are in an advanced state of decomposition. Recently, proteomics studies using animal models have identified potential biomarkers for PMI and AAD estimation. This study investigated the human bone proteome in four human body donors studied throughout decomposition outdoors. We compared different bone tissues (tibia and iliac crest) from body donors of known AAD, and compared bone samples taken shortly after death to bone samples upon complete skeletonization of the body. The effects of ageing phenomena (in vivo and post-mortem) and the surrounding environment on the variability and abundancy of the bone proteome were assessed.
2021-09-09 | PXD019693 | Pride
Project description:Horses receiving antimicrobials may develop diarrhea due to changes in the gastrointestinal microbiome and metabolome. This matched, case-controlled study compared the fecal microbiome and metabolome in hospitalized horses on antibiotics that developed diarrhea (AAD), hospitalized horses on antibiotics that did not develop diarrhea (ABX) and a healthy, non-hospitalized control population (CON). Naturally-voided fecal samples were collected from AAD horses (n=17) the day that diarrhea developed and matched to ABX (n=15) and CON (n=31) horses for diet, antimicrobial agent and duration of antimicrobial therapy (< 5 days or > 5 days). Illumina sequencing of 16S rRNA genes on fecal DNA was performed. Alpha and beta diversity metrics were generated using QIIME 2.0. A Kruskal-Wallis with Dunn’s post-test and ANOSIM testing was used for statistical analysis. Microbiome composition in AAD was significantly different from CON (ANOSIM, R= 0.568, p=0.001) and ABX (ANOSIM, R=0.121, p=0.0012). Fecal samples were lyophilized and extracted using a solvent-based method. Untargeted metabolomics using gas chromatography-mass spectrometry platforms was performed. Metabolomic data was analyzed using Metaboanalyst 4.0 and Graphpad Prism v 7. Principal component analysis plots (PCA) were used to visualize the distribution of metabolites between groups. Heat maps were used to identify the relative concentrations amongst the most abundant 25 metabolites. A one-way ANOVA was used to compare differences in metabolites amongst the three groups of horses. Only named metabolites were included in the analysis. The microbiome of AAD and ABX horses had significantly decreased richness and evenness than CON horses (p<0.05). Actinobacteria (q=0.0192) and Bacteroidetes (q=0.0005) were different between AAD and CON. Verrucomicrobia was markedly decreased in AAD compared to ABX and CON horses (q=0.0005). Horses with AAD have a dysbiosis compared to CON horses, and show minor differences in bacterial community composition to ABX horses. Metabolite profiles of horses with AAD clustered separately from those with AAD or CON. Ten metabolites were found to be significantly different between groups (P<0.05) and are listed according to their metabolic pathway: amino acid metabolism (R-equol, L-tyrosine, kynurenic acid, xanthurenic acid, 5-hydroxyindole-3-acetic acid ) lipid metabolism (docosahexaenoic acid ethyl ester), biosynthesis of secondary metabolites (daidzein, isoquinoline) and two metabolites with unidentified pathways (1,3-divinyl-2-imidazolidinone, N-acetyltyramine).
2021-03-10 | ST001823 | MetabolomicsWorkbench