Analysis of aortic gene expression in mice with aortic dissection treated with colchicine
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ABSTRACT:
PROVIDER: PRJNA1173225 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31004457_1.fastq.gz | Fastqsanger.gz | |||
| SRR31004457_2.fastq.gz | Fastqsanger.gz | |||
| SRR31004458_1.fastq.gz | Fastqsanger.gz | |||
| SRR31004458_2.fastq.gz | Fastqsanger.gz | |||
| SRR31004459_1.fastq.gz | Fastqsanger.gz |
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Project description:Colchicine is an alkaloid found in the plant Colchicum, which is currently used for the treatment of acute gout and familial Mediterranean fever, and is being considered for the treatment of a variety of cardiovascular diseases such as pericarditis, atrial fibrillation, and coronary syndromes due to its significant anti-inflammatory effects. Aortic dissection is a cardiovascular disease characterised by a tear in the intima and congestion of the vessel wall leading to vessel wall delamination, with a rapid onset and high lethality. This study investigated the role of colchicine in BAPN-induced aortic dissection in mice. Gavage administration of colchicine along with BAPN modelling for three weeks showed a significant decrease in morbidity and mortality, indicating that colchicine can inhibit the occurrence of aortic dissection in mice.
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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).
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Project description:The mechanisms of acute aortic dissection are not well understood. Transcriptomic strategy has been proven to be an effective way to find the potential mechanisms and also the reliable biomarkers for a specific disease. The whole-genome expression profiling was assayed in a panel of aortic tissues from 4 male acute aortic dissection patients and 4 male healthy controls.
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Project description:Purpose: The aim of this study is to have a fullscape of molecular pathology of Stanford type A aortic dissection Methods: All TAAD patients under consideration underwent an ascending aortic replacement surgery during a cardiopulmonary bypass. The normal ascending aortic tissue samples were obtained from patients undergoing coronary artery bypass grafting surgery (CABG) without any aortic diseases. We selected 20 samples (10 TAAD and 10 normal) for the whole transcriptome sequencing. Total RNA was extracted from each sample using TRIzol Reagent (ThermoFisher) and was stored in 1 mL of 75% ethanol at -80 ℃ until further usage. Conclusions: We identified exaggerated autophagy as a molecular biomarker for aortic dissection. We also predicted 10 hub genes and an HIF1A-ATG3 axis which could provide new insights in understanding aortic dissection.
2020-07-02 | GSE153434 | GEO
Project description:Expression data from control, aortic aneurysm, and aortic dissection cells
| PRJNA907394 | ENA
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