Differential gene expression in M. tuberculosis infected-murine bone marrow-derived macrophages upon colchicine treatment
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ABSTRACT:
PROVIDER: PRJNA760787 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15720433.fastq.gz | Fastqsanger.gz | |||
| SRR15720434.fastq.gz | Fastqsanger.gz | |||
| SRR15720435.fastq.gz | Fastqsanger.gz | |||
| SRR15720436.fastq.gz | Fastqsanger.gz | |||
| SRR15720437.fastq.gz | Fastqsanger.gz |
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Project description:We investigated the molecular mechanisms by which colchicine regulates host defense in macrophages against M. tuberculosis infection. To elucidate this, we performed global gene expression analysis of M. tuberculosis infected-bone marrow-derived macrophages after colchicine treatment.
2021-09-11 | GSE183440 | GEO
Project description:Doxorubicin (DOX) cardiotoxicity is an important factor of heart failure. The only clinically approved drug is dexrazoxane, while its side effect of secondary malignancies severely limited its application. It is urgent to find other alternative efficacious molecular for these chemotherapy patients. Colchicine is a safe and well tolerated anti-inflammation drug which also functions in attenuating the reactive oxygen species (ROS) generation. High dose of colchicine was reported block the autophagosome-lysosome fusion in cancer cells due to its destabilization effect to the microtubule system, while how colchicine affects the autophagic flux in cardiomyocytes is largely unknown. Recent years low dose of colchicine administration was reported helpful to the patients with pericarditis, postprocedural atrial fibrillation and coronary artery disease, most of the research attributed it to its anti-inflammation effect. Whether the autophagic flux regulated by colchicine also benefits to DOX induced heart failure remains unclear. Doxorubicin (DOX) administration was used to establish heart failure models in vivo and in vitro. Results showed that DOX blocked the autophagic vacuoles degradation, leading to damaged mitochondria and ROS accumulation. Heart failure characteristics were obviously improved after low dose of colchicine administration. Mechanistically, low dose of colchicine promoted the autolysosome degradation, cleared the damaged mitochondria, and ROS accumulation induced by the DOX and as a result attenuated DOX cardiotoxicity.
2024-06-20 | GSE247345 | GEO
Project description:Differential gene expression in murine bone marrow-derived macrophages upon GABA treatment
| PRJNA454829 | ENA
Project description:Objective. Colchicine is an alkaloid that is used to alleviate acute gout and to prevent acute attacks of familial Mediterranean fever (FMF). However, it is not beneficial when given during the occurrence of an acute episode of FMF. It is believed that colchicine exerts its anti-inflammatory effect through direct interaction with microtubules. We aim to study the molecular basis of colchicine action by analysing the effect of this drug on global gene expression of HUVEC (human umbilical vein endothelial cell line) cells. Methods. HUVEC cells were exposed to various concentrations of colchicine and were harvested at different time points. Ribonucleic acid was extracted, amplified, reverse transcribed and hybridized to complementary deoxyribonucleic acid microarrrays containing more than 40,000 probes to human expressed sequence tags. This approach enabled us to have a global look at the transcriptional response induced by colchicine treatment. Results. Colchicine changed the expression of many genes in HUVEC cells following exposure to a concentration of 100 ng/ml or higher. Following short exposure (30 or 120 min), colchicine affected genes known to be involved in the cell cycle and its regulation. However, change in expression of genes involved in neutrophil migration or other inflammatory processes were observed mainly after 12 to 24 h. Conclusions. The anti-inflammatory effect of colchicine may be mediated not only through direct interaction with microtubules but also through changes at the transcriptional level. This latter effect apparently requires a higher concentration and a longer time to occur. This can explain the observation that colchicine does not have an immediate effect when given during an acute attack of FMF. A dose response design type examines the relationship between the size of the administered dose and the extent of the response of the organism(s). Keywords: dose_response_design
2006-01-25 | GSE4090 | GEO
Project description:Objective. Colchicine is an alkaloid that is used to alleviate acute gout and to prevent acute attacks of familial Mediterranean fever (FMF). However, it is not beneficial when given during the occurrence of an acute episode of FMF. It is believed that colchicine exerts its anti-inflammatory effect through direct interaction with microtubules. We aim to study the molecular basis of colchicine action by analysing the effect of this drug on global gene expression of HUVEC (human umbilical vein endothelial cell line) cells. Methods. HUVEC cells were exposed to various concentrations of colchicine and were harvested at different time points. Ribonucleic acid was extracted, amplified, reverse transcribed and hybridized to complementary deoxyribonucleic acid microarrrays containing more than 40,000 probes to human expressed sequence tags. This approach enabled us to have a global look at the transcriptional response induced by colchicine treatment. Results. Colchicine changed the expression of many genes in HUVEC cells following exposure to a concentration of 100 ng/ml or higher. Following short exposure (30 or 120 min), colchicine affected genes known to be involved in the cell cycle and its regulation. However, change in expression of genes involved in neutrophil migration or other inflammatory processes were observed mainly after 12 to 24 h. Conclusions. The anti-inflammatory effect of colchicine may be mediated not only through direct interaction with microtubules but also through changes at the transcriptional level. This latter effect apparently requires a higher concentration and a longer time to occur. This can explain the observation that colchicine does not have an immediate effect when given during an acute attack of FMF. A dose response design type examines the relationship between the size of the administered dose and the extent of the response of the organism(s). Using regression correlation
2006-01-24 | E-GEOD-4090 | biostudies-arrayexpress
Project description:Objective. Colchicine is an alkaloid that is used to alleviate acute gout and to prevent acute attacks of familial Mediterranean fever (FMF). However, it is not beneficial when given during the occurrence of an acute episode of FMF. It is believed that colchicine exerts its anti-inflammatory effect through direct interaction with microtubules. We aim to study the molecular basis of colchicine action by analysing the effect of this drug on global gene expression of HUVEC (human umbilical vein endothelial cell line) cells. Methods. HUVEC cells were exposed to various concentrations of colchicine and were harvested at different time points. Ribonucleic acid was extracted, amplified, reverse transcribed and hybridized to complementary deoxyribonucleic acid microarrrays containing more than 40,000 probes to human expressed sequence tags. This approach enabled us to have a global look at the transcriptional response induced by colchicine treatment. Results. Colchicine changed the expression of many genes in HUVEC cells following exposure to a concentration of 100 ng/ml or higher. Following short exposure (30 or 120 min), colchicine affected genes known to be involved in the cell cycle and its regulation. However, change in expression of genes involved in neutrophil migration or other inflammatory processes were observed mainly after 12 to 24 h. Conclusions. The anti-inflammatory effect of colchicine may be mediated not only through direct interaction with microtubules but also through changes at the transcriptional level. This latter effect apparently requires a higher concentration and a longer time to occur. This can explain the observation that colchicine does not have an immediate effect when given during an acute attack of FMF.
2005-10-07 | E-SMDB-3505 | biostudies-arrayexpress
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.
2024-10-25 | GSE279545 | GEO
Project description:Mycobacterium tuberculosis infection of mice elicits a robust neutrophil influx that associates with poor outcome from tuberculosis (TB). However, the mechanism by which neutrophils contribute to TB disease pathogenesis is not understood. To gain insights into the pathological functions of neutrophils, the current study performs bulk mRNA sequencing from the neutrophils isolated from lung, spleen and bone marrow of resistant (C57BL/6) and susceptible (IL-1R1 KO) mice at 28 days post M.tuberculosis HN878 infection.
2024-02-29 | GSE203118 | GEO
Project description:The aim of this study was to identify the signaling pathways differentially engaged upon infection with either live or heat killed Mycobacterium tuberculosis in murine bone marrow derived macrophages. Based on preliminary data that type I IFN signaling dominates the transcriptional differences, we investigated what roles the type I IFN receptor IFNAR and the signaling molecule STING play during infection with either live or heat killed Mycobacterium tuberculosis in bone marrow derived macrophages. In WT and STING KO macrophages, IFNbeta treatment was added either by itself or in addition to both of the infection conditions to test whether the lack of IFNbeta induction in these cells accounted for any differences in transcriptional respones.added IFNbeta treatment either by itself or in addition to both of the infection conditions.
2021-03-29 | GSE162620 | GEO
Project description:Time-course transcriptional profiling of IFNg-primed C57/BL6 and C3H.BL6-sst1 bone-marrow macrophages infected with mycobacterium tuberculosis (MTB)
2010-01-07 | E-MTAB-90 | biostudies-arrayexpress