Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA206434 | ENA |
REPOSITORIES: ENA
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Project description:CSB ablation induced apoptosis is mediated by Increased Endoplasmic Reticulum Stress Response: a gene expression study
| PRJNA325696 | ENA
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
2013-06-04 | GSE47591 | GEO
Project description:Bronchopulmonary dysplasia (BPD), a chronic lung disease of prematurity, has been linked to endoplasmic reticulum (ER) stress. To investigate a causal role for ER stress in BPD pathogenesis, we generated mice (cGrp78f/f) with lung epithelial cell-specific knockout (KO) of Grp78, a gene encoding the ER chaperone 78-kDa glucose-regulated protein (GRP78), a master regulator of ER homeostasis and the unfolded protein response (UPR). Lung epithelial-specific Grp78 KO disrupted lung morphogenesis, causing developmental arrest, increased alveolar epithelial type II cell apoptosis and decreased surfactant protein and type I cell marker expression in perinatal lungs. cGrp78f/f pups died immediately after birth, likely due to respiratory distress. Importantly, Grp78 KO triggered UPR activation with marked induction of pro-apoptotic transcription factor C/EBP homologous protein (CHOP). Increased expression of genes involved in oxidative stress and cell death and decreased expression of genes encoding antioxidant enzymes suggest a role for oxidative stress in alveolar epithelial cell (AEC) apoptosis. Increased Smad3 phosphorylation and expression of transforming growth factor-β (TGF-β)/Smad3 targets Cdkn1a (encoding p21) and Gadd45a suggest that interactions among the apoptotic arm of the UPR, oxidative stress and TGF-β/Smad signaling pathways contribute to Grp78 KO-induced AEC apoptosis and developmental arrest. Chemical chaperone taursodeoxycholic acid reduced UPR activation and apoptosis in cGrp78f/f lungs cultured ex vivo, confirming a role for ER stress in observed AEC abnormalities. These results demonstrate a key role for GRP78 in AEC survival and gene expression during lung development through modulation of ER stress and suggest the UPR as a potential therapeutic target in BPD. Whole-genome expression profiling was performed using MouseRef-8 v2.0 Expression BeadChips (Illumina) on RNA isolated from lungs of four Grp78f/f and three cGrp78f/f mice at E18.
2016-01-15 | E-GEOD-70208 | biostudies-arrayexpress
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.
2013-06-04 | E-GEOD-47591 | biostudies-arrayexpress
Project description:Bronchopulmonary dysplasia (BPD), a chronic lung disease of prematurity, has been linked to endoplasmic reticulum (ER) stress. To investigate a causal role for ER stress in BPD pathogenesis, we generated mice (cGrp78f/f) with lung epithelial cell-specific knockout (KO) of Grp78, a gene encoding the ER chaperone 78-kDa glucose-regulated protein (GRP78), a master regulator of ER homeostasis and the unfolded protein response (UPR). Lung epithelial-specific Grp78 KO disrupted lung morphogenesis, causing developmental arrest, increased alveolar epithelial type II cell apoptosis and decreased surfactant protein and type I cell marker expression in perinatal lungs. cGrp78f/f pups died immediately after birth, likely due to respiratory distress. Importantly, Grp78 KO triggered UPR activation with marked induction of pro-apoptotic transcription factor C/EBP homologous protein (CHOP). Increased expression of genes involved in oxidative stress and cell death and decreased expression of genes encoding antioxidant enzymes suggest a role for oxidative stress in alveolar epithelial cell (AEC) apoptosis. Increased Smad3 phosphorylation and expression of transforming growth factor-β (TGF-β)/Smad3 targets Cdkn1a (encoding p21) and Gadd45a suggest that interactions among the apoptotic arm of the UPR, oxidative stress and TGF-β/Smad signaling pathways contribute to Grp78 KO-induced AEC apoptosis and developmental arrest. Chemical chaperone taursodeoxycholic acid reduced UPR activation and apoptosis in cGrp78f/f lungs cultured ex vivo, confirming a role for ER stress in observed AEC abnormalities. These results demonstrate a key role for GRP78 in AEC survival and gene expression during lung development through modulation of ER stress and suggest the UPR as a potential therapeutic target in BPD.
2016-01-15 | GSE70208 | GEO
Project description:Study of the effects of the VCP knockdown. VCP (p97, yeast cdc48) is a hexameric AAA ATPase involved in various cellular functions including degradation of proteins by the ubiquitin-proteasome system. We examine the consequences of the reduction of VCP levels after RNAi of VCP in HeLa cells. We find ~30 transcripts upregulated in a sequence independent manner. Those transcripts encode proteins involved in endoplasmic reticulum stress, apoptosis, and amino acid starvation.
2006-08-23 | E-MEXP-817 | biostudies-arrayexpress
Project description:Ethnopharmacological relevance: Helicobacter pylori (H.pylori) infection is the leading cause of gastric mucosal damage and inflammation, and persistent infection is one of the major risk factors for gastric cancer. Eradication of H.pylori remains a clinical challenge, and therefore, it is urgently necessary to identify more drugs that can interfere with H.pylori colonization and promote its clearance. Jiawei Lianpu Yin (JWLPY) is a compound formula composed of natural drugs used to treat gastric diseases associated with H.pylori infection. However, the underlying mechanisms of its action are still unclear. Aim of the study: The aim of this study was to investigate whether JWLPY can inhibits H.pylori colonization and alleviates gastric mucosal inflammation and damage and to explore its mechanism of action. Materials and METHODS: The effects of JWLPY on Helicobacter pylori and gastric mucosa injury were studied by using Helicobacter pylori induced gastritis model in rats. Transcriptomics, network pharmacology and bioinformatics were used to determine the mechanism of JWLPY Results: JWLPY inhibited the aggregation of inflammatory cells and preserved the integrity of the mucosal barrier, reducing autophagy and apoptosis in gastric mucosal epithelial cells. Network pharmacology and transcriptomics analysis revealed that JWLPY promotes the assembly and synthesis of MUC5AC in the endoplasmic reticulum by activating the IRE1-XBP1 signaling pathway, which enhances the process of protein assembly in the endoplasmic reticulum, thereby inhibiting H.pylori colonization in the gastric mucosa. Conclusion: This study is the first to demonstrate that JWLPY inhibits H.pylori colonization in the gastric mucosa, alleviates gastric inflammation and damage, and is a potential drug for the treatment of H.pylori -related gastritis.
2025-04-03 | GSE293658 | GEO
Project description:Epithelial endoplasmic reticulum stress orchestrates a protective IgA response I
| PRJNA512503 | ENA
Project description:Epithelial endoplasmic reticulum stress orchestrates a protective IgA response II
| PRJNA512502 | ENA
Project description:Gene expression profiling of kidneys from the murine model of HIV-associated nephropathy (HIVAN) identified an association between the expression of an endoplasmic reticulum (ER)-associated protein reticulon-1, RTN1, and the severity of kidney disease. Of the three known RTN1 isoforms, only RTN1A protein expression was increased in kidneys of murine models of HIVAN, diabetic nephropathy (DN), and renal fibrosis and humans with HIVAN and DN. Both mRNA and protein expression of RTN1-A in the kidneys correlated inversely with estimated glomerular filtration rate (eGFR) in patients with DN. In kidney cells, RTN1 overexpression induced ER stress/apoptosis, whereas RTN1 knockdown attenuated tunicamycin-, and hyperglycemia-induced ER stress/apoptosis. Incubation of kidney cells with high glucose media induced RTN1A expression likely through oxidative pathway, while knockdown of RTN1A inhibited high glucose-induced apoptosis. RTN1A interacts with PERK and mutation of its N- or C-terminal domain abolished its effects on ER stress/apoptosis. In vivo, knockdown of Rtn1a expression either before or after kidney injury attenuated renal fibrosis in mice with unilateral ureteral obstruction (UUO) and tubular epithelial cell-specific knockdown of Rtn1a also ameliorated ER stress and renal fibrosis in the UUO mice. Finally, knockdown of Rtn1a also attenuated proteinuria, glomerular hypertrophy, and mesangial expansion in STZ-induced diabetic mice, which were associated with suppression of ER stress markers. Taken together, these data suggest that RTN1 is a mediator of kidney disease progression that exacerbates kidney injury through ER stress and apoptosis.
2015-05-20 | GSE69074 | GEO