Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Total RNA-seq of rat living myocardial slices (LMS) treated with aloxistiatin (E64d)

ABSTRACT: This study aims to explore the therapeutic potential of the cysteine protease inhibitor aloxistatin (E64d) as a candidate to combat cardiac fibrotic progression. Rodent living myocardial slices (LMS) from left ventricular tissue were treated for 4h and 24h with aloxistatin (100µM) or DMSO control. For RNA isolation from LMS, LMS were transferred into 2ml vials containing ceramic beads and QiAzol Lysis reagent and tissue was homogenized utilizing the Precellys Evolution. RNA isolation was performed based on phenol-chloroform-extraction method.

INSTRUMENT(S): Illumina NovaSeq X

ORGANISM(S): Rattus norvegicus

SUBMITTER: Kevin Schmidt

PROVIDER: E-MTAB-16035 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Effect of ferrostatin-1 on living myocardial slices derived from heart failure patients

Project description:Cardiac injury remains a leading cause of death globally with limited availability of therapeutic approaches. In this study, we employed living myocardial slices (LMS) as an ex vivo model of cardiac injury to investigate underlying mechanisms and potential therapeutic targets. Cryoinjury was induced in adult rat LMS, resulting in 30% tissue damage. Cryoinjured LMS demonstrated impaired contractile function, cardiomyocyte hypertrophy, inflammation, and cardiac fibrosis, closely resembling in vivo cardiac injury characteristics. Proteomic analysis revealed an enrichment of factors associated with ferroptosis in the injured LMS, suggesting a potential causative role. To test this hypothesis, we pharmacologically inhibited ferroptosis using ferrostatin (Fer-1) in the cryoinjured rat LMS, resulting in attenuation of structural changes and repression of pro-fibrotic processes. Furthermore, LMS generated from failing human hearts were used as a model of chronic heart failure. In this model, Fer-1 treatment was observed to reduce the expression of ferroptotic genes and enhance contractile function. Blocking ferroptosis in human cardiac fibroblasts (HCFs) resulted in a downregulation of fibroblast activation genes, a decrease in fibroblast migration capacity, and a reduction in reactive oxygen species production. Analysis of RNA sequencing data from Fer-1-treated human LMS revealed that metallothioneins, a group of cysteine-rich proteins recognized for their antioxidative attributes and capacity to neutralize free radicals and reactive oxygen species, might serve as a potential mechanism underlying the suppression of ferroptosis. This effect is likely to be mediated by replenishing the existing glutathione reserves within the cells, which are then harnessed to combat lipid peroxidation and ferroptosis. These findings highlight the potential of targeting ferroptosis and metallothioneins as a promising strategy for the treatment of heart disease.

2024-10-02 | GSE243655 | GEO

Synergistic effects of TRAIL and taurolidine on soft tissue sarcoma cell lines

Project description:Microarray analysis revealed differential gene expression patterns of rhabdomyosarcoma (A-204), leiomyosarcoma (SK-LMS-1) and epithelioid cell sarcoma (VA-ES-BJ) cells treated with TRAIL and/or taurolidine. To explore new therapeutic options in the treatment of sarcomas, we tested the antibiotic taurolidine (TRD) on A-204, SK-LMS-1 and VA-ES-BJ carcinoma cell lines alone and in combination with rhTRAIL (TNF related apoptosis-inducing ligand). Gene expression was analysed by RNA microarray. Cell lines were treated with Taurolidine, Trail and a combination of both and compaired to untreated cells

2013-03-17 | E-GEOD-36572 | biostudies-arrayexpress

RNA-seq of patients with aplastic anemia in the presence or absence of levamisole in vitro

Project description:Bone marrow nucleated cells (BMNCs) from healthy donors and patients with non-severe aplastic anemia (NSAA) at the time of initial diagnosis were separated, and then co-cultured with or without 40 μg/mL levamisole (LMS) for 48 hours in vitro. Cells were harvested and total RNA were extracted. The sequencing assay were carried out using the Illumina HiSeq X platform and the data obtained were analyzed by following the Hisat2 protocol.

2024-07-11 | E-MTAB-11942 | biostudies-arrayexpress

mRNA-seq of human cardiac fibrobasts (HCF) profibrotic stimulated with TGFb and treated with aloxistatin (E64d)

Project description:This study aimed to explore the therapeutic potential of the cysteine protease inhibitor aloxistatin (E64d) as a candidate to combat cardaic fibrotic progression. Human cardiac fibroblasts (HCFs) derived from diseased myocardium including ischemic and dilated cardiomyopathies (ICM, DCM) were treated for 48 h with 100 µM aloxistatin or DMSO control and pro-fibrotic stimulated with 5 ng/mL TGFβ1 or respective vehicle (veh) control (4 mM HCl containing 0.1% bovine serum albumin). HCF were harvested with QiAzol Lysis reagent (Qiagen) and RNA was isolated based on phenol-chloroform-extraction procedure.

2026-07-06 | E-MTAB-16034 | biostudies-arrayexpress

Total RNA-seq of rat living myocardial slices (LMS) treated with aloxistiatin (E64d)

Project description:Total RNA-seq of rat living myocardial slices (LMS) treated with aloxistiatin (E64d)

| PRJEB102531 | ENA

Expression data of bone marrow-derived osteoclasts expressing wild-type or mutant PSS1

Project description:Phosphatidylserine (PS) is an acidic phospholipid that is involved in various cellular events. Heterologous dominant mutations have been identified in the gene encoding PS synthase 1 (PSS1) in patients of a congenital disease called Lenz-Majewski syndrome (LMS). LMS patients show various symptoms, including craniofacial/distal-limb bone dysplasia and progressive hyperostosis. The LMS-causing gain-of-function mutants of PSS1 (PSS1-LMS) have been shown to synthesize PS without control, but why the uncontrolled synthesis would lead to LMS is unknown. We investigated the effect of PSS1-LMS(Q353R) on osteoclasts to elucidate the causative mechanism of LMS and found that PSS1-LMS inhibited the formation, multinucleation, and activity of osteoclasts. We used microarrays to comprehensively examine the effects of PSS1-LMS on osteoclast gene expression.

2022-07-04 | GSE207351 | GEO

Stratification of Leiomyosarcoma molecular subtypes by 3' end RNA-sequencing: Toward precision medicine

Project description:Leiomyosarcoma (LMS) is a malignant neoplasm with smooth muscle differentiation. Little is known about its molecular heterogeneity and no targeted therapy currently exists for LMS. We demonstrate the existence of 3 molecular subtypes in a cohort of 99 cases and an independent cohort of 82 LMS. Two new FFPE tissue-compatible diagnostic immunohistochemical markers are identified: LMOD1 for subtype I LMS and ARL4C for subtype II LMS. Subtype I and subtype II LMS are associated with good and poor prognosis, respectively. The LMS subtypes show significant differences in expression levels for genes for which novel targeted therapies are being developed.

2015-05-19 | GSE45510 | GEO

Oncogenic gene expression programs in leiomyosarcoma and characterization of conventional, inflammatory and uterogenic subtypes

Project description:Leiomyosarcoma (LMS) is a mesenchymal neoplasm with complex copy number alterations and characteristic loss of tumor suppressor genes without known recurrent activating mutations. Clinical management of advanced LMS relies on chemotherapy and complementary palliative approaches, and research efforts to date have had limited success identifying clinically actionable biomarkers or targeted therapeutic vulnerabilities. To explore the biological underpinning of LMS, we evaluated gene expression patterns of this disease in comparison to diverse sarcomas, non-mesenchymal neoplasms and normal myogenic tissues. We identified a recurrent gene expression program in LMS, with evidence of oncogenic evolution of an underlying smooth muscle lineage-derived program characterized by activation of E2F1 and downstream effectors. Recurrently amplified or highly expressed genes in LMS were identified that may represent therapeutic vulnerabilities, including targeting of IGF1R and retinoid signaling pathways. Though the majority of expressed transcripts were conserved across LMS samples, three separate subtypes were identified that were enriched for muscle-associated transcripts (conventional-LMS), immune markers (inflammatory-LMS) or a uterine-like gene expression program (uterogenic-LMS). Each of these subtypes express a unique subset of genes that may be useful in the managemeny of LMS: IGF1R was enriched in conventional LMS with prognostic implications, worse disease-specific survival was observed in inflammatory LMS, and prolactin was elaborated by uterogenic LMS and may represent a disease biomarker. These results extend our understanding of LMS biology and identify several strategies and challenges for further translational investigation.

2020-06-09 | GSE146360 | GEO

Phialemonium globosum strain:LMS 16-13

Project description:Phialemonium globosum LMS 16-13 Transcriptome - LMS 16-13

| PRJNA1360844 | ENA

Genomic and Histologic Analysis of Uterine Leiomyosarcoma from Leiomyoma with Bizarre Nuclei

Project description:Leiomyoma with bizarre nuclei (LM-BN) is a rare variant of leiomyoma with a benign clinical course. In contrast, leiomyosarcoma (LMS) is a high-grade, malignant neoplasm characterized by high recurrence rates and poor survival. While LM-BN and LMS show distinct morphologies, they share similar immunoprofile and molecular alterations, with both considered “DNA unstable”. Rare cases of LM-BN associated with LMS have been reported, however the histogenesis and molecular relationship between these two tumors remains unclear. In this study, we assessed 11 cases of LMS arising in conjunction with LM-BN and further analyzed the clinical, histologic, and molecular characteristics of these lesions. Tumor slides were examined by histology and immunohistochemistry to confirm the presence of both LMS and LM-BN components. LM-BN and LMS had similar p16 and p53 IHC patterns, but LMS had a higher Ki-67 index and lower ER/PR expression. Digital image analysis based on nuclear and cytologic features revealed spatial relationships between LMS and LM-BN. Genomic copy number alteration (CNA) demonstrated the same clonal origin of LMS from existing LM-BN through conserved copy number alterations. LMS harbored higher CNAs and frequent loss of the TP53, Rb, PTEN, and/or CDKN2A genomic region than LM-BN, indicative of tumor progression. Spatial transcriptome analysis defined uniquely expressed gene signatures in a geographical distribution, demonstrating molecular evidence of regional cell specific differences of LM-BN and LMS. Mutation analysis of large oncogenic panel revealed many shared functional gene alterations in both LM-BN and LMS, but more highly enriched in LMS. Our findings for the first time suggest that a subset of LMS arise from an existing LM-BN.

2024-11-05 | GSE270865 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data