Sprr2f protects against renal injury by decreasing the level of reactive oxygen species in female mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA641162 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12071729_1.fastq.gz | Fastqsanger.gz | |||
| SRR12071729_2.fastq.gz | Fastqsanger.gz | |||
| SRR12071730_1.fastq.gz | Fastqsanger.gz | |||
| SRR12071730_2.fastq.gz | Fastqsanger.gz | |||
| SRR12071731_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Renal injury leads to chronic kidney disease for which women are not only more likely to be diagnosed with than men but also have poorer outcomes as well. We have previously shown that expression of Sprr2f, a member of the Small Proline Rich Region (Sprr) gene family, is increased several hundred fold after renal injury using a unilateral ureter obstruction (UUO) mouse model. To better understand the role of Sprr2f in renal injury, we generated a Sprr2f knockout (Sprr2f-KO) mouse model using CRISPR-Cas9 technology. To identify genes that are differentially expressed in Sprrf2f-KO mice after UUO, we performed gene expression profiling by RNA-seq on kidney tissues harvested from Sprr2f-KO mice at time 0 (n=4) and after 5 days (n=3), a time known to show dramatic changes in gene expression. Compared to day 0, expression levels of 162 genes were significantly changes with 121 up-regulated and 41 down-regulated 5 days after obstruction. Enrichment analysis using PANTHER Classification System identified 12 and 2 pathways enriched in genes that are upregulated or downregulated after UUO respectively. Eleven out of the 12 pathways enriched in the genes upregulated after UUO are related to metabolism such as drug metabolic process, consistent with a profound role of kidney as a major clearance organ of the body responsible for the elimination of many xenobiotics and prescription drugs. Interestingly, the only pathway not related to metabolism enriched in genes upregulated by UUO is oxidation-reduction, suggesting a potential role of oxidative stress in renal damage after UUO in Sprr2-KO animals. This phenotype is not observed in Sprr2f-WT animals after UUO in our previous gene expression profiling study, suggesting that Sprr2f function is sufficient to protect kidney from oxidative damage after UUO in Sprr2f-WT animals.
2020-10-13 | GSE153010 | GEO
Project description:Renal injury leads to chronic kidney disease, with which women are not only more likely to be diagnosed than men but have poorer outcomes as well. We have previously shown that expression of small proline-rich region 2f (Sprr2f), a member of the small proline-rich region (Sprr) gene family, is increased several hundredfold after renal injury using a unilateral ureteral obstruction (UUO) mouse model. To better understand the role of Sprr2f in renal injury, we generated a Sprr2f knockout (Sprr2f-KO) mouse model using CRISPR-Cas9 technology. Sprr2f-KO female mice showed greater renal damage after UUO compared with wild-type (Sprr2f-WT) animals, as evidenced by higher hydroxyproline levels and denser collagen staining, indicating a protective role of Sprr2f during renal injury. Gene expression profiling by RNA sequencing identified 162 genes whose expression levels were significantly different between day 0 and day 5 after UUO in Sprr2f-KO mice. Of the 162 genes, 121 genes were upregulated after UUO and enriched with those involved in oxidation-reduction, a phenomenon not observed in Sprr2f-WT animals, suggesting a protective role of Sprr2f in UUO through defense against oxidative damage. Consistently, bilateral ischemia-reperfusion injury resulted in higher serum blood urea nitrogen levels and higher tissue reactive oxygen species in Sprr2f-KO compared with Sprr2f-WT female mice. Moreover, cultured renal epithelial cells from Sprr2f-KO female mice showed lower viability after oxidative damage induced by menadione compared with Sprr2f-WT cells that could be rescued by supplementation with reduced glutathione, suggesting that Sprr2f induction after renal damage acts as a defense against reactive oxygen species.
| S-EPMC7789986 | biostudies-literature
Project description:Renal Proximal Tubular Cells of young / senescent replicative age or high / low reactive oxygen species content were profiled using an Affymetrix Chip Platform.<br>Sample classifications: <br>Young refers to the in vitro age of early passage cells. <br>Senescent indicates cells at the end of their in vitro life span, having entered an irreversible growth arrest. <br>SortHI refers to cells with high intracellular reactive oxygen species content that were sorted by FACS according to a bright FL1 fluorescence after staining with 1 ï¾µM CM-H2DCFDA (Molecular Probes Cat No C6827).<br>SortLO refers to cells with low intracellular reactive oxygen species content that were sorted by FACS according to a dim FL1 fluorescence after staining with 1 ï¾µM CM-H2DCFDA.<br>
2011-01-15 | E-MEXP-2683 | biostudies-arrayexpress
Project description:To identify components involved in the signal transduction and activation of the singlet oxygen-mediated response, a mutant selection was performed. This led to the isolation of the singlet oxygen resistant 1 (sor1) mutant, which is more tolerant to singlet oxygen-producing chemicals and shows a constitutively higher expression of GPXH and GSTS1. Map-based cloning revealed that the SOR1 gene encodes a novel bZIP transcription factor, which seems to control its own expression as well as that of a large number of oxidative stress response and detoxification genes. In the promoter region of many of these genes a highly conserved 8-bp palindromic sequence element was found to be enriched. This element was shown to be essential for GSTS1 overexpression in sor1 and for induction by increased levels of lipophilic reactive electrophile species (RES) suggesting that it functions as an electrophile response element (ERE). RES can be formed after singlet oxygen-induced lipid peroxidation, indicating that a RES-stimulated and SOR1-mediated response of detoxification genes is part of the singlet oxygen-induced acclimation process in C. reinhardtii. The sor1 mutant isolated in a screen for singlet oxygen resistant mutants and the corresponding wild-type strain 4A+ were grown in a 12 h light dark cycle for several days before total RNA was extracted 6 h after the light came on.
2012-04-03 | E-GEOD-33548 | biostudies-arrayexpress
Project description:Phytochrome B regulates reactive oxygen signaling during stress in plants.
| PRJNA780007 | ENA
Project description:To identify components involved in the signal transduction and activation of the singlet oxygen-mediated response, a mutant selection was performed. This led to the isolation of the singlet oxygen resistant 1 (sor1) mutant, which is more tolerant to singlet oxygen-producing chemicals and shows a constitutively higher expression of GPXH and GSTS1. Map-based cloning revealed that the SOR1 gene encodes a novel bZIP transcription factor, which seems to control its own expression as well as that of a large number of oxidative stress response and detoxification genes. In the promoter region of many of these genes a highly conserved 8-bp palindromic sequence element was found to be enriched. This element was shown to be essential for GSTS1 overexpression in sor1 and for induction by increased levels of lipophilic reactive electrophile species (RES) suggesting that it functions as an electrophile response element (ERE). RES can be formed after singlet oxygen-induced lipid peroxidation, indicating that a RES-stimulated and SOR1-mediated response of detoxification genes is part of the singlet oxygen-induced acclimation process in C. reinhardtii.
2012-04-03 | GSE33548 | GEO
Project description:Metabolic determinants of cellular fitness dependent on mitochondrial reactive oxygen species
| PRJNA663327 | ENA
Project description:mitochondrial electron transport in Arabidopsis leaves was blocked by antimycin A treatment to trigger mitochondrial production of reactive oxygen species and to study transcriptional changes in response
2010-12-31 | E-TABM-641 | biostudies-arrayexpress
Project description:Wollbold2014 - Effects of reactive oxygen
species
This model is described in the article:
Anti-inflammatory effects of
reactive oxygen species ¿ a multi-valued logical model
validated by formal concept analysis.
Wollbold J, Jaster R, Müller S,
Rateitschak K, Wolkenhauer O.
BMC Syst Biol 2014 Sep; 8(1): 101
Abstract:
BackgroundRecent findings suggest that in pancreatic acinar
cells stimulated with bile acid, a pro-apoptotic effect of
reactive oxygen species (ROS) dominates their effect on
necrosis and spreading of inflammation. The first effect
presumably occurs via cytochrome C release from the inner
mitochondrial membrane. A pro-necrotic effect ¿ similar to
the one of Ca2+ ¿ can be strong opening of mitochondrial
pores leading to breakdown of the membrane potential, ATP
depletion, sustained Ca2+ increase and premature activation of
digestive enzymes. To explain published data and to understand
ROS effects during the onset of acute pancreatitis, a model
using multi-valued logic is constructed. Formal concept
analysis (FCA) is used to validate the model against data as
well as to analyze and visualize rules that capture the
dynamics.ResultsSimulations for two different levels of bile
stimulation and for inhibition or addition of antioxidants
reproduce the qualitative behaviour shown in the experiments.
Based on reported differences of ROS production and of ROS
induced pore opening, the model predicts a more uniform
apoptosis/necrosis ratio for higher and lower bile stimulation
in liver cells than in pancreatic acinar cells. FCA confirms
that essential dynamical features of the data are captured by
the model. For instance, high necrosis always occurs together
with at least a medium level of apoptosis. At the same time,
FCA helps to reveal subtle differences between data and
simulations. The FCA visualization underlines the protective
role of ROS against necrosis.ConclusionsThe analysis of the
model demonstrates how ROS and decreased antioxidant levels
contribute to apoptosis. Studying the induction of necrosis via
a sustained Ca2+ increase, we implemented the commonly accepted
hypothesis of ATP depletion after strong bile stimulation.
Using an alternative model, we demonstrate that this process is
not necessary to generate the dynamics of the measured
variables. Opening of plasma membrane channels could also lead
to a prolonged increase of Ca2+ and to necrosis. Finally, the
analysis of the model suggests a direct experimental testing
for the model-based hypothesis of a self-enhancing cycle of
cytochrome C release and ROS production by interruption of the
mitochondrial electron transport chain.
This model is hosted on
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MODEL1407230001.
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2015-04-15 | MODEL1407230001 | BioModels
Project description:In this study, we investigated the impact of PZH on inducing reactive oxygen species (ROS) to inhibit colorectal cancer (CRC) growth. CRC cell line HCT116 was exposed to PZH for 24 hours, then RNA-Sequencing was conducted and showed that PZH modulated ROS-related signaling pathways, including DNA repair and the unfolded protein response, concomitant with the suppression of proliferation-related genes such as PCNA and Ki-67.
2023-10-19 | GSE245680 | GEO