Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA254518 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptome response to endoplasmic reticulum stress in rat oligodendrocyte precursor cells
| PRJNA322543 | ENA
Project description:Myeloperoxidase (MPO), oxidative stress (OS), and endoplasmic reticulum (ER) stress are all increased in the lungs of neonatal rat pups raised in hyperoxia (HOX, >90% O2), an established model of bronchopulmonary dysplasia (BPD). However, the relationship between OS, MPO, and ER stress has not been examined in HOX rat pups. To determine the relationship between OS, MPO, and ER stress in BPD we treated Sprague-Dawley neonatal rat pups with Tunicamycin (Tun) or with HOX. Tun directly induces ER stress and simplifies neonatal lung alveolarization. Previously, we showed that HOX induces a cycle of destruction that we hypothesize through increased OS, MPO, and ER stress to induce BPD. To inhibit ER stress specifically, we used tauroursodeoxycholic acid (TUDCA), a molecular chaperone. To break the cycle of destruction and reduce OS and MPO we used N-acetyl-lysyltyrosylcysteine-amide (KYC), a systems pharmacology agent. Lung structure was studied morphometrically. ER stress was detected using immunofluorescence (IF), transcriptomic, proteomic, and electron microscopic analyses. Increased ER stress was observed in the lungs of HOX rat pups and also in human BPD lungs by IF. Morphometric and proteomic studies of rat lungs showed that Tun treatment decreased lung complexity and increased ER stress and BPD severity. The fact that TUDCA improved lung complexity in Tun-treated neonatal rat pups, and decreased BPD induced by HOX provides strong support for the idea that ER stress plays a causal role in BPD. Additional support comes from data showing TUDCA decreased lung myeloid cells and MPO levels in the lungs of both Tun- and HOX-treated neonatal rat pups. These data link OS and MPO to ER stress in the mechanisms mediating BPD. KYC's effective inhibition of ER stress in the lungs of Tun-treated rat pups provides additional support for the idea that MPO-induced ER stress plays a direct causal role in BPD. Thus, ER stress appears to expand our proposed cycle of destruction. Our results suggest ER stress evolves from OS and MPO to increase neonatal lung injury and impaired neonatal lung growth and development. The encouraging effect of TUDCA indicates chemical chaperone has the potential in treating BPD. Using multiomic data to investigate the role of endoplasmic reticulum stress in the development of BPD in rat model.
2022-08-11 | GSE197403 | GEO
Project description:To investigate whether ER stress underpins the secretion of mis-glycosylated glycoproteins by trophoblast, we treated trophoblast-like BeWo cells with the ER stress inducer thapsigargin (Tg), an inhibitor specific for sarco/endoplasmic reticulum Ca2+-ATPase.
2022-12-04 | E-MTAB-10943 | biostudies-arrayexpress
Project description:AtbZIP60 is one of the transcription factors involved in the endoplasmic reticulum (ER) stress response in Arabidopsis. To identify genes under the control of AtbZIP60 during ER stress, we compared the genome-wide expression profiles of wild-type and atbzip60 mutant plants in response to the ER stress inducer tunicamycin.
2008-11-19 | E-MEXP-1753 | biostudies-arrayexpress
Project description:Effects of calcitriol on expressions of ER stress related genes were evaluated with microarray. Calcitriol, the active form of vitamin D, is known to induce apoptosis in cancer cells and increase intracellular calcium. Increase in cytopalsmic calcicium levels may indicate a decrease in endoplasmic reticulum (ER) calcium levels since ER is the main storage unit for calcium. Decrease in ER calcium levels are known to induce ER stress which can lead to apoptosis. However the effects of calcitriol on ER stress have not been reported before. Here we hypotesized that the cellular effects of calcitriol can be explained by induction of ER stress. We have tested this hypothesis by assessing calcitriol induced transcriptomic alterations with a focus on ER stress related genes.
2015-01-01 | GSE53975 | GEO
Project description:Oxidative stress (OS), inflammation, and endoplasmic reticulum (ER) stress sequentially occur in the rat model of hyperoxia (HOX) induced bronchopulmonary dysplasia (BPD), and they all increase DNA damage. Tumor suppressors increase after DNA damage, followed by apoptosis or cellular senescence when the damage becomes irreparable. Although cellular senescence contributes to wound healing, its persistence will inhibit growth potential. Therefore, we hypothesized that the persistence of cellular senescence plays a role in BPD progression. We detected evidence of increased cellular senescence in rat and human BPD lungs. Foxo4-p53 binding was increased in BPD rat lungs, and inhibition of this binding attenuated BPD severity, indicating that such binding contributes to BPD's cellular senescence. Treatment with tauroursodeoxycholic acid (TUDCA) decreases ER stress. N-Acetyl-lysyltyrosylcysteine-amide (KYC) reduced toxic oxidant production by myeloperoxidase (MPO) and subsequent OS and inflammation. Both agents effectively decreased cellular senescence. Concomitantly, alveolar complexity and the number of type 2 alveolar cells increased, indicating that MPO-mediated OS and ER stress preceded cellular senescence in BPD rat pup lungs. These data suggest that cellular senescence plays an essential role in BPD progression. Reducing MPO toxic oxidant production, ER stress, and attenuating cellular senescence are potential therapeutic strategies for halting BPD progression. Using multiomic data to investigate the role of cellular senescence in the development of BPD in rat model.
2024-01-01 | GSE223745 | GEO
Project description:Endoplasmic reticulum (ER) stress, a disruption of ER homeostasis, is involved in the pathophysiology of several human diseases, including metabolic dysfunction-associated steatotic liver disease (MASLD). MASLD, formerly known as nonalcoholic fatty liver disease (NAFLD), is characterized by an excessive accumulation of hepatic lipids. To characterize ER stress-induced changes in the expression of genes involved in lipid metabolism, HepG2 human hepatoma cells were exposed to tunicamycin, followed by transcriptome profiling. Among genes involved in lipid biosynthesis, GPAT3 was strongly activated by tunicamycin while many other genes involved in this process (e.g., DGAT2, AGPAT2, AGPAT3, GPAT1, DGAT1 and GPAT4) were downregulated. Since GPAT proteins catalyze rate-limiting step in the de novo synthesis of glycerophospholipids and triglycerides, the unique expression pattern of GPAT3 potentially links it to ER stress-associated accumulation of lipids in hepatic cells.
2025-12-10 | GSE296996 | GEO
Project description:The endoplasmic reticulum (ER) is the site of secretory lipoprotein production and de novo cholesterol synthesis, yet little is known about how these activities are coordinated with each other, or with the activity of the COPII machinery, which transports ER cargo to the Golgi. The Sar1B component of this machinery is mutated in Chylomicron Retention Disorder, establishing that this Sar1 isoform secures delivery of dietary lipids into the circulation. We used microarrays to investigate the effect of overexpression of Sar1 isoforms and a constitutively active mutant form of Sar1B, Sar1B:H79G, on global gene expression in rat hepatoma cell line, McArdle RH7777 and identified a strong down-regulation of cholesterol biosynthetic gene mRNA expression in the Sar1B:H79G-, but not the wild-type Sar1A- or Sar1B-overexpressing cell lines. RNA was extracted from cell cultures of control McArdle RH7777, and transgenic lines overexpressing human Sar1-isoforms: one for Sar1A, two for Sar1B and two expressing a constitutively active mutant form of Sar1B, Sar1B:H79G, that cannot complete GTP hydrolysis, and hybridized on Affymetrix GeneChip Rat Genome 230 2.0 arrays.
2013-12-16 | E-GEOD-52969 | biostudies-arrayexpress
Project description:Endoplasmic reticulum (ER) stress and the unfolded protein response (UPR)
| PRJNA137213 | ENA
Project description:The endoplasmic reticulum (ER) is the site of secretory lipoprotein production and de novo cholesterol synthesis, yet little is known about how these activities are coordinated with each other, or with the activity of the COPII machinery, which transports ER cargo to the Golgi. The Sar1B component of this machinery is mutated in Chylomicron Retention Disorder, establishing that this Sar1 isoform secures delivery of dietary lipids into the circulation. We used microarrays to investigate the effect of overexpression of Sar1 isoforms and a constitutively active mutant form of Sar1B, Sar1B:H79G, on global gene expression in rat hepatoma cell line, McArdle RH7777 and identified a strong down-regulation of cholesterol biosynthetic gene mRNA expression in the Sar1B:H79G-, but not the wild-type Sar1A- or Sar1B-overexpressing cell lines.
2013-12-16 | GSE52969 | GEO