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A Transcriptomics-Based Computational Drug Repositioning Pipeline Identifies Simvastatin And Primaquine As Novel Therapeutics For Endometriosis Pain

ABSTRACT: A Transcriptomics-Based Computational Drug Repositioning Pipeline Identifies Simvastatin And Primaquine As Novel Therapeutics For Endometriosis Pain

PROVIDER: PRJNA1261874 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR33529501_1.fastq.gz	Fastqsanger.gz
	SRR33529501_2.fastq.gz	Fastqsanger.gz
	SRR33529503_1.fastq.gz	Fastqsanger.gz
	SRR33529503_2.fastq.gz	Fastqsanger.gz

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A Transcriptomics-Based Computational Drug Repositioning Pipeline Identifies Simvastatin And Primaquine As Novel Therapeutics For Endometriosis Pain

Project description:Endometriosis is a disease with limited medical treatment options and a strong need for new therapeutic strategies. We previously applied a transcriptomics-based computational drug repositioning pipeline to publicly available bulk transcriptomic data to identify potential therapeutics for endometriosis. The drug candidates identified in silico includes fenoprofen, primaquine, and simvastatin. Validation of these drugs in our rat endometrial model determined that they significantly reduced endometriosis-associated vaginal hyperalgesia, a surrogate marker for endometriosis-related pain. The signatures of DEGs from uteri and lesions demonstrated reversal of the endometriosis disease signature with simvastatin and primaquine treatment.

2025-06-25 | GSE296883 | GEO

Transcriptomic Repositioning Analysis Identifies mTOR Inhibitor as Potential Therapy for Epidermolysis Bullosa Simplex

Project description:In this study, we characterize significant molecular pathways activated in the blisters that form in EBS and employ a systematic drug repositioning screen to identify promising repositionable drugs for EBS. We implicate the PI3K/AKT/mTOR pathway as central in the EBS disease pathway and further validate our computational repositioning analysis by presenting clinical outcomes of two EBS patients treated with mTOR inhibitors.

2021-07-09 | GSE179508 | GEO

Effect of simvastatin on pancreatic cancer cells

Project description:The aim of our study was to assess the impact of simvastatin on the amount of cytosolic lipid droplets (LDs), which are implicated in many biological processes including proliferation, inflammation, carcinogenesis, apoptosis, necrosis or growth arrest. Human pancreatic cancer cells MiaPaCa-2 were treated with simvastatin (6 and 12 _M) for 24 hours. Changes in expression of genes related to lipid metabolism in the simvastatin-treated cells were examined by DNA microarray analysis. The treatment of the cells with simvastatin increased their intracellular content of LDs, partially due to the uptake of cholesterol and triacylglycerides from medium; but in particular, due to enhanced synthesis of triacylglycerides as proved by detection of significant overexpression of genes related to de novo synthesis of triacylglycerides and phospholipids. Further, simvastatin markedly influenced expression of genes directly affecting cell proliferation and signaling.

2013-11-21 | E-MTAB-1501 | biostudies-arrayexpress

Computational drug repositioning identifies niclosamide and tribromsalan as inhibitors of Mycobacterium tuberculosis and Mycobacterium abscessus

Project description:Computational drug repositioning identifies niclosamide and tribromsalan as inhibitors of Mycobacterium tuberculosis and Mycobacterium abscessus

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Simvastatin modulates osteogenic differentiation in stem cells isolated from apical papilla

Project description:Background Simvastatin modulates numerous stem cell functions, including stemness maintenance and differentiation. The present study aimed to explore the effect of simvastatin on the osteogenic differentiation of SCAPs in vitro. Methods Cells were isolated from apical papilla, and mesenchymal stem cell features were characterised. Cells were treated with various concentrations of simvastatin (100-1,000 nM). The mRNA expression profile of simvastatin-treated SCAPs was examined using RNA sequencing technique. The osteogenic differentiation abilities were assessed. Alkaline phosphatase activity was determined. The mineralisation was visualised using Alizarin Red S and Von Kossa staining. The osteogenic marker gene expression was determined using a quantitative polymerase chain reaction. Results RNA sequencing data demonstrated that simvastatin upregulated genes enriched in those pathways involving osteogenic differentiation, including the TGF-beta signalling pathway, FoxO signalling pathway, and MAPK signalling pathway, while the downregulated genes were involved in pathways related to cell proliferation and apoptosis, for example, DNA replication, cell cycle, and p53 signalling pathway. Simvastatin promoted mineral deposition in a dose-dependent manner, corresponding with the upregulation of osteogenic marker genes namely OSX, DMP1, DSPP, and OCN. Pretreatment with TGF-beta receptor inhibitor, SB431542, resulted in a moderately attenuated effect on simvastatin-induced mineralisation and osteogenic marker gene expression. Conclusions Simvastatin enhances osteogenic differentiation in SCAPs, potentially via TGF-beta signalling, implicating its potential role as an adjunctive molecule in dental pulp healing and regeneration in vital pulp treatment approaches.

2025-01-22 | GSE286540 | GEO

Transcriptomic profiling of simvastatin-treated human umbilical vein endothelial cells

Project description:We report that simvastatin induces an immunoregulatory transcriptional profile in endothelial cells that is potent to modulate CD4+ T cell biology.

2021-10-28 | GSE171123 | GEO

Simvastatin has an anti-inflammatory effect on macrophages via upregulation of Kruppel-like factor-2

Project description:HMG-CoA reductase inhibitors, statins, have beneficial vascular effects beyond their cholesterol-lowering action. These pleiotropic effects include an anti-inflammatory effect on macrophages. Since macrophages play a central role in atherogenesis, we further characterized the effects on peripheral blood monocyte-macrophages (HPBM). Using Affymetrix gene chip analysis of simvastatin-treated HPBM, we found that simvastatin treatment lead to the downregulation of the expression of many proinflammatory genes including several chemokines (e.g. MCP-1, MIP-1 alpha and β, RANTES, several other CC and CXC chemokines, IL-2 receptor-β, and leukemia inhibitory factor), members of the tumor necrosis factor family (e.g. lymphotoxin beta and TRAIL), VCAM-1, ICAM-3, and tissue factor (TF). Simvastatin also modulated the expression of several transcription factors essential for the inflammatory response: simvastatin downregulated the expression of NF-kappaB relA/p65 subunit and ets-1 transcription factor, and upregulated the expression of a novel atheroprotective transcription factor, Kruppel-like factor 2 (KLF-2). The effects of simvastatin on KLF-2 and its target genes were dependent on protein prenylation, since inhibitors of protein prenylation had a similar inhibitory effect in THP-1 derived macrophages. Additionally, by lentiviral overexpression KLF-2 we showed that the effect of simvastatin on MCP-1 and TF were dependent on KLF-2. We concluded that simvastatin had a strong anti-inflammatory effect on macrophages, which includes upregulation of the atheroprotective transcription factor KLF-2. These findings further explain the beneficial pleiotropic effects of statins on cardiovascular diseases. Keywords: time-course, response to treatment

2006-12-31 | GSE4883 | GEO

Gene expression profiling of human neuroblastoma cell line SMS-KCNR treated with DMSO, simvastatin at 5 µM or simvastatin at 5 µM plus mevalonate at 2 mM for 30 hours

Project description:Microarray gene expression profiling reveals that simvastatin regulates the expression of M phase cell cycle genes and mevalonate metabolism

2023-05-01 | GSE215949 | GEO

Simvastatin treated Lymphoblastoid Cell lines from Cholesterol and Pharmacogenomics (CAP) Trial

Project description:Statins reduce cardiovascular disease risk by lowering plasma low density lipoprotein (LDL)-cholesterol. To identify novel pathways that modulate statin response, we assessed the influence of simvastatin exposure on expression quantitative trait locus (eQTL) associations across the genome in 480 lymphoblastoid cell lines (LCLs). Cell lines were derived blood samples collected ant entry visit from participants in the Cholesterol and Pharmacogenomics (CAP) trial, who underwent a 6 week 40mg/day simvastatin trial. We identified 4590 cis-eQTLS that were independent of treatment status (FDR=1%) and six cis-eQTLS for which there was evidence of an interaction with treatment (FDR=20%). Genotypes and Phenotypes derived from these indivudals are available through dbGaP (Accession Number). eQTL results are available at: http://eqtl.uchicago.edu/cgi=bin/gbrowse/eqtl/ Dataset consists of 960 expression beadarrays (Illumina HumanRef-8v3) representing paired samples derived from 24-hour exposures of 480 lymphoblastoid cell lines (LCLs) to 2 micromolar simvastatin acid or control buffer.

2012-06-30 | E-GEOD-36868 | biostudies-arrayexpress

SIMVASTATIN ATTENUATES LIVER INJURY IN RODENTS WITH BILIARY CIRRHOSIS SUBMITTED TO HEMORRHAGE/RESUSCITATION

Project description:In variceal bleeding liver function deterioration is a major cause of death. The effects of bleeding on intrahepatic microvascular dysfunction, which contributes to liver injury in cirrhosis, are largely unknown. The aims of this study were to evaluate the impact of hemorrhage/resuscitation (H/R) on cirrhotic microcirculation, and whether simvastatin, a drug that improves liver microcirculation, has hepatoprotective effects. The study was performed in three groups of rats: controls, rats with biliary cirrhosis (CBDL) and CBDL rats pre-treated with 3 doses (5 mg*Kg-1*day-1) of simvastatin. Rats were submitted to H/R or sham procedure. Subsequently, livers were isolated and perfused for functional assessment of liver microcirculation. Liver transcriptome was assessed with microarrays. H/R significantly impaired endothelial-dependent vasorelaxation in cirrhotic (p=0.035) but not control livers. H/R induced a similar increase in ALT in control and cirrhotic rats, whereas the increase in AST was 10 times higher in cirrhotic than in control rats (p=0.007). Simvastatin prevented the impairment in endothelial-dependent vasorelaxation induced by H/R, and reduced by half the increase in ALT and AST (p<0.05). Transcriptomics showed a marked upregulation of genes related to inflammatory response after H/R in cirrhotic livers, but not in controls, and this was blunted by simvastatin. In conclusion, H/R aggravates liver microvascular dysfunction in cirrhosis, and upregulates liver inflammatory pathways. This does not occur in control livers. Simvastatin prevented H/R-induced liver endothelial dysfunction, and attenuated liver injury and liver inflammatory response, suggesting that it might have potential for protecting the cirrhotic liver during bleeding complications.

2016-12-22 | GSE84178 | GEO

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