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Ginsenoside Rd monomer alleviates ulcerative colitis by regulating miRNAs and target genes in macrophages

ABSTRACT: to discover the miRNAs involved in the production of cytokines by RAW264.7 cells treated with LPS and ginsinoside Rd monomer We then performed gene expression profiling analysis using data obtained from RNA-seq of RAW264.7 cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE231990 | GEO | 2024/04/01

REPOSITORIES: GEO

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Haemophilus influenzae Rd KW20 strain:Rd

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Outer membrane vesicle and outer membrane of Haemophilus influenzae Rd KW20, Rd ∆yrbE and Rd ∆vacJ

Project description:Bacterial outer membrane vesicles (OMVs) have important biological roles in pathogenesis and intercellular interactions, but a general mechanism of OMV formation is lacking. Here we show that the VacJ/Yrb ABC transport system, a proposed phospholipid (PL) transporter, is involved in OMV formation. Deletion or repression of VacJ/Yrb increases OMV production in two distantly related Gram-negative bacteria, Haemophilus influenzae and Vibrio cholerae. Within our studies we also analyzed the proteome of the OMV and outer membrane (OM) and found no massive alteration in Haemophilus influenzae Rd KW20, Rd ∆yrbE and Rd ∆vacJ. Lipidome analyses demonstrate that OMVs from VacJ/Yrb-defective mutants in H. influenzae are enriched in PLs and certain fatty acids. Furthermore, we demonstrate that OMV production and regulation of the VacJ/Yrb ABC transport system respond to iron starvation. Our results suggest a new general mechanism of OMV biogenesis based on PL accumulation in the outer leaflet of the outer membrane. This mechanism is highly conserved among Gram-negative bacteria, provides a means for regulation, can account for OMV formation under all growth conditions, and might have important pathophysiological roles in vivo.

2016-01-27 | PXD003249 | Pride

RD effect on PC-3 cells

Project description:RD induced DNA damage and suppressed DNA repair in PC-3 cells. Expression profiling of PC-3 cells treated with 10 umol/L RD for 24 hours.

2012-05-08 | GSE37812 | GEO

RD effect on PC-3 cells

Project description:RD induced DNA damage and suppressed DNA repair in PC-3 cells. Expression profiling of PC-3 cells treated with 10 umol/L RD for 24 hours. Total RNA was extracted from PC-3 cells exposed to RD for 24 h using an RNAiso plus kit (TaKaRa). Microarray analysis was performed on separate samples on the Affymetrix HG-U133 plus 2 chip.

2012-05-07 | E-GEOD-37812 | biostudies-arrayexpress

Homo sapiens Ewing sarcoma cell line RD-ES: Negative control vs. HDGF knockdown

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Homo sapiens Ewing sarcoma cell line RD-ES: Negative control vs. HDGF knockdown

Project description:Comparing the gene expression profiling of HDGF-silenced RD-ES cells and control RD-ES cells to identify genes regulated by HDGF in RD-ES cells. Keywords: expression analysis Control RD-ES cells and HDGF-silenced RD-ES cells were profiled on 22K Human Genome Array

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Specific immunotherapy plus Clostridium butyricum alleviates ulcerative colitis in patients with food allergy.

Project description: Not available

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Gene expression data from DMD patient hiPSC-derived myoblasts treated with fenofibrate, ginsenoside Rd or DMSO

Project description:Drug development costs a significant amount of time and resources for new pharmaceutical drugs. However, the progress has been limited for orphan diseases such as Duchenne muscular dystrophy (DMD). By using human induced pluripotent stem cells (hiPSCs), here we show an exemplary drug screening campaign and the identification of two potential drugs effective in a DMD mouse model. We developed a DMD-hiPSC screening platform utilizing high-content imaging to identify hit compounds that enhance myogenic fusion abilities of patient-specific myoblasts. Among 1524 compounds (Johns Hopkins Clinical Compound library), two hit compounds restored in vitro fusion defects of DMD patient hiPSC-derived myoblasts. Transcriptional profiling revealed that the function of two hit compounds, ginsenoside Rd (natural product, ginseng extract) and fenofibrate (FDA-approved drug), are associated with FLT3 signaling and TGF-β signaling, respectively. The preclinical tests in mdx mice show that the treatment of the two hit compounds can ameliorate the skeletal muscle and behavioral phenotypes caused by DYSTROPHIN deficiency, suggesting therapeutic potential of these two compounds. Our study demonstrates the feasibility of early-stage drug development for rare diseases using symptom-relevant cells derived from patient-specific hiPSCs.

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