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ChIP-seq analysis of changes in H3K27ac by endoplasmic reticulum stress (ERS) in mouse primary hepatocytes.

ABSTRACT: ChIP-seq analysis of changes in H3K27ac by endoplasmic reticulum stress (ERS) in mouse primary hepatocytes.

PROVIDER: PRJNA505776 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8197280.fastq.gz	Fastqsanger.gz
	SRR8197281.fastq.gz	Fastqsanger.gz
	SRR8197282.fastq.gz	Fastqsanger.gz
	SRR8197283.fastq.gz	Fastqsanger.gz
	SRR8197276.fastq.gz	Fastqsanger.gz

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ChIP-seq analysis of changes in H3K27ac by endoplasmic reticulum stress (ERS) in mouse primary hepatocytes.

Project description:Mouse primary hepatocytes (MPH) prepared from C57Bl6 male adult mice were treated with the ERS-drug thapsigargin and ChIP-seq was performed using an H3K27ac antibody (Active Motif ref 39685).

2020-04-29 | GSE122613 | GEO

Transcriptomic analysis of endoplasmic reticulum stress (ERS) regulated genes in mouse primary hepatocytes.

Project description:Transcriptomic analysis of endoplasmic reticulum stress (ERS) regulated genes in mouse primary hepatocytes.

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Transcriptomic analysis of endoplasmic reticulum stress (ERS) regulated genes in mouse primary hepatocytes.

Project description:Mouse primary hepatocytes (MPH) prepared from C57Bl6 male adult mice were treated with the ERS-drug thapsigargin and used to prepare RNA.

2020-04-29 | GSE122507 | GEO

Hepatocytes cyclooxygenase-2 deficiency improves liver injury via inhibition of endoplasmic reticulum stress and epithelial-mesenchymal transition

Project description:The mechanism underlying the loss of normal liver tissues in liver cirrhosis, mainly hepatocytes, is not well-characterized. Endoplasmic reticulum (ER) stress-induced cell death has emerged as a potential mechanism for chronic liver diseases. We have previously demonstrated that cyclooxygenase-2 (COX-2) is closely related to the progress of liver cirrhosis. In this study, we aimed to verify whether hepatocytes COX-2 deficiency could protect liver injury via inducing ER stress in liver cirrhosis.

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Transcriptomic and epigenomic analysis of endoplasmic reticulum stress signaling in mouse primary hepatocytes and liver

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Transcriptomic analysis of endoplasmic reticulum stress (ERS) regulated genes in mouse gastrocnemius muscle

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Combination of Eribulin and Anlotinib Exerts Synergistic Cytotoxicity in Retroperitoneal Liposarcoma by Inducing Endoplasmic Reticulum Stress

Project description:Primary retroperitoneal liposarcoma (RLPS) is a rare heterogeneous tumor occurring within retroperitoneal space, and its overall survival did not improve much in the past few decades. Based on a small-sample clinical practice at our center, patients with RLPS can greatly benefit from combination of anlotinib and eribulin. In this study, we investigated combinational effect of anlotinib and eribulin on RLPS. Through transcriptome analysis, we uncovered and validated that synergistic effect mainly induced by endoplasmic reticulum stress (ERS) pathway both in vitro and in vivo.

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Extracellular vesicles from human umbilical cord mesenchymal stem cells protect grafted islets against endoplasmic reticulum stress-induced mitochondrial dysfunction by modulating XBP1-based calcium homeostasis

Project description:Islet transplantation is an ideal option for diabetes while early graft lose serves as a major obstacle. Human umbilical cord mesenchymal stem cells (hucMSC) have multiple functions including the maintenance of cellular homeostasis. However, it is unknown whether extracellular vesicles (EVs) derived from hucMSC (hucMSC-EVs) provide protective effects against transplant-related trauma-induced islet injury. Here, we isolated and purified hucMSC-EVs, and found that hucMSC-EVs promoted grafted islet survival, and enhanced glycemic control following co-transplantation in a syngeneic streptozotocin (STZ)-induced mouse model of diabetes. After co-cultured for 12 h or 24 h, labelled hucMSC-EVs with PKH67 were readily internalized by NIT-1 β cells and islets. In tunicamycin (Tm) and thapsigargin (Tg) induced specific endoplasmic reticulum stress (ERS) cell injury models, hucMSC-EVs treatment improved cell viability and β cells function both in NIT-1 cells and ex vivo primary islets. Bulk RNA-seq demonstrated that hucMSC-EVs treatment significantly involved in ERS and the negative regulated mitochondrial apoptotic pathway. While ERS promoted interactions between endoplasmic reticulum (ER) and mitochondria, hucMSC-EVs alleviated ERS, maintained calcium homeostasis, and improved mitochondrial energy metabolism. Notably, the downregulation of XBP1 by hucMSC-EVs fine-tuned ER-mitochondria communication via reducing inositol-1,4,5-trisphosphate receptors at mitochondria-associated membranes (MAMs). Reduced XBP1 also activated Nrf2, restoring mitochondrial calcium homeostasis under ERS. miRNA analysis identified miR-182-5p enriched in hucMSC-EVs that specifically targeted XBP1 mRNA, leading to its degradation and downregulation. These findings demonstrate that hucMSC-EVs protect grafted islets by blocking XBP1 and restoring calcium homeostasis, thus suggesting their potential as a cell-free therapy for improving islet transplantation outcomes.

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2011-12-20 | E-GEOD-31539 | biostudies-arrayexpress

Tunicamycin-induced Endoplasmic Reticulum-Quality Control Pathway and Endoplasmic Reticulum-Associated Degradation Mechanism in the diatom Phaeodactylum tricornutum

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