Project description:Clopidogrel is associated with a series of gastrointestinal side effects, such as bleeding complications and recurrent gastric ulcer; however, their mechanisms are largely unclear. In this study, human gene expression microarray and gene ontology analysis were utilized to evaluate the effects of clopidogrel on gene expression in human gastric epithelial cells (GES-1) Keywords: Clopidogrel; Gastric injury; GES-1 cell line
Project description:Clopidogrel is associated with a series of gastrointestinal side effects, such as bleeding complications and recurrent gastric ulcer; however, their mechanisms are largely unclear. In this study, human gene expression microarray and gene ontology analysis were utilized to evaluate the effects of clopidogrel on gene expression in human gastric epithelial cells (GES-1) Keywords: Clopidogrel; Gastric injury; GES-1 cell line The Agilent Whole Human Genome Oligo Microarray was measured at 24 hours after GES-1 cells were exposure to clopidogrel ( 1.5mmol/l). The experimental set up the control group and the clopidogrel group. Three chips were performed on each group.
Project description:In this study, cultured H.pylori was used to infect the normal gastric epithelial cell line GES-1, to construct the H.pylori infection model. lncRNA microarray was applied for detecting the lncRNA in H.pylori infection model.
Project description:Research on lncRNAs expression profiles in human interactions with Helicobacter pylori (H.pylori) is rare reported. We used HTA2.0 to investigate the expression changes of lncRNAs and mRNAs in human gastric epithelial cells (GES-1 cell line) infected with or without H.pylori infection. Our study provided a preliminary exploration of lncRNAs expression profiles in H.pylori-infected cell models by microarray. A subset of aberrantly expressed lncRNAs was verified by qRT-PCR. These dysregulated lncRNAs might contribute to the pathological processes during H.pylori infection.
Project description:Research on lncRNAs expression profiles in human interactions with Helicobacter pylori (H.pylori) is rare reported. We used HTA2.0 to investigate the expression changes of lncRNAs and mRNAs in human gastric epithelial cells (GES-1 cell line) infected with or without H.pylori infection. Our study provided a preliminary exploration of lncRNAs expression profiles in H.pylori-infected cell models by microarray. A subset of aberrantly expressed lncRNAs was verified by qRT-PCR. These dysregulated lncRNAs might contribute to the pathological processes during H.pylori infection. We infected GES-1 cells with H.pylori as experimental groups,and cells without H.pylori infection were regarded as control groups. After 24hr-infection, cells of each group were selected for total RNA extraction and hybridization on Affymetrix HTA2.0 arrays. The aberrant expression profiles of lncRNAs and mRNAs were explored by microarray analysis between experimental and control groups.
Project description:To analyze the gene expression of human gastric epithelial cells (GES-1) regulated by paeonifl or in based on transcript tome sequencing; to identify and analyze key genes; to study the mechanism of paeoniflorin on Leuk-1cells; and to explore its medicinal value. Method: Different doses of Ulcer-healing Decoction were used to treat GES-1, and its activity was assessed by MTT assay. Transcriptome sequencing analysis was then performed to identify differentially expressed genes (DEGs). The function and pathways of the DEGs were annotated using GO and KEGG enrichment analysis. Result: The survival rate of GES-1 cells was significantly increased under different concentrations of ulcer-healing decoction intervention (P < 0.05 or P < 0.01). After 24 hours of treatment with 80 µ g/mL ulcer-healing decoction, a total of 312 crucial DEGs were observed in GES-1 cells, of which 233 DEGs were upregulated and 79 DEGs were downregulated. The top five differentially expressed genes include CYP1A1, IL24, IKBKGP1, GDF15, SCUBE1 and OASL, ADAMTS5, SULF1, ID2, and DDX60. The functions of these genes are mainly related to promoting wound,cell proliferation and migration,immunity and inflammation.GO enrichment analysis showed that the DEGs were significantly enriched in the extracellular region and involved in biological processes such as cytokine production and response, stimulus response, and exerting molecular functions such as proliferation factor receptor activity. KEGG pathway enrichment showed that the DEGs were significantly enriched in various signaling pathways. Immunohistochemistry and other methods were used to detect differentially expressed proteins in GES-1 cells induced by ulcer-healing decoction, and the results were consistent with those from RNA-seq, thereby validating the accuracy of sequencing technologies. Conclusion: The role of ulcer-healing decoction in GES-1 is primarily reflected in regulating inflammatory factors and growth factors, promoting cell proliferation, and supporting the regeneration and repair of gastric mucosal epithelial cells.
Project description:With the colonization of Helicobacter Pylori (H.pylori) in the human stomach, a large amount of Helicobacter Pylori (H.pylori)colonized into the stomach disintegrates and releases a large number plenty of toxic proteins and other bacterial structure components. TollToll-like receptors (TLRs) in gastric epithelial cells which sensitive to the components of bacteria lysate around the microenvironment attach them and activite innate immune and pro-inflammatory response once contact with antigen. The consequences after long-term stimulation of H.pylori lysate in gastric epithelial cells has not been reported . To investigate the effects of H.pylori lysate on TLRs expression and inflammatory cytokines level during long-term stimulation of gastric epithelial cells and clarify the potential mechanismHence, we detected TLRs mRNA level and inflammatory cytokines expression in GES-1 cells co-culture with lysate from 1 to 30 generations. The sensitivity to H.pylori or H.pylori lysate in GES-1 cells were also monitored. We also explored whether LPS was the main factors contributing to this change. Mongolian gerbils were used to replicate H.pylori infection animal model. After transcriptome sequencing,A TLR2/6 heterodimers agonist Pam2CSK4 and a highly selective inhibitor of PI3K LY294002 were used to clarify the TLR6 signaling pathways. In a conclusion, we discovered that the sensitivity of TLRs in human gastric epithelial cells decreased while after long-time co-culture with H.pylori lysate. Human gastric epithelial cells shows tolerance to H.pylori lysate in TLRs and inflammatory cytokines level. decreased the high level of TLRs and inflammatory cytokines after stimulating GES-1 cells with H.pylori lysate for a short-term. And Tthis process may works through the TLR6/PI3K/NF-κKB axis.
Project description:The phase 3 ZUMA-7 trial in second-line large B-cell lymphoma demonstrated superiority of anti-CD19 CAR T-cell therapy (axicabtagene ciloleucel; axi-cel) over standard of care (SOC; salvage chemotherapy followed by hematopoietic transplantation). Here, we present a prespecified exploratory analysis examining the association between pretreatment tumor characteristics and the efficacy of axi-cel versus SOC. B-cell gene expression signature (GES) and CD19 expression significantly associated with improved event-free survival (EFS) for axi-cel (P=.0002 for B-cell GES; P=.0165 for CD19 expression) but not SOC (P=.9374 for B-cell GES; P=.5526 for CD19 expression). Axi-cel showed superior EFS over SOC irrespective of B-cell GES and CD19 expression (P=8.56e–9 for B-cell GES high; P=.0019 for B-cell GES low; P=3.85e–9 for CD19 gene high; P=.0017 for CD19 gene low). Low CD19 expression in malignant cells correlated with a tumor GES consisting of immune suppressive stromal and myeloid genes, highlighting the inter-relation between malignant cell features and immune contexture substantially impacting axi-cel outcomes. Tumor burden, lactate dehydrogenase, and cell-of-origin impacted SOC more than axi-cel outcomes. T-cell activation and B-cell GES, which are associated with improved axi-cel outcome, decreased with increasing lines of therapy. These data highlight differences in resistance mechanisms to axi-cel and SOC and support earlier intervention with axi-cel.