Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1284538 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Our preliminary data suggest that differential gut microbiota modulates acetaminophen-induced hepatotoxicity (APAP toxicity) in mice model. The goal of our study is to determine whether commensal gut microbiota modulates the hepatic gene expressions potentially responsible for modulating APAP toxicity.
2025-01-10 | GSE125418 | GEO
Project description:Investigation of the effect of chow diet integration with standard baker's yeast leavened carasau bread (SB) or with functional sourdough-leavened carasau bread (FB) on the gut microbiota of young rats.
2019-08-19 | PXD011441 | Pride
Project description:Background: Tissue kallikrein-related peptidases 4, 5, 6 and 7 (KLK4-7) strongly increase the malignancy of ovarian cancer cells. By further deciphering the downstream effectors of KLK4-7, we aimed at finding new potential prognostic biomarkers and treatment targets for ovarian cancer patients. KLK4-7-transfected and vector-control OVMZ-6 (OV-KLK4-7 and OV-VC) ovarian cancer cells were established to select differentially regulated factors. Methods: Three independent approaches, PCR arrays, genome-wide microarray and proteome analyses, were pursued leading to the identification of ten candidates (MSN, KRT19, COL5A2, COL1A2, BMP5, F10, KRT7, JUNB, BMP4, MMP1). Differential gene expression in OV-KLK4-7 versus OV-VC cells was validated by qPCR. To determine differential protein expression, Western blot analyses, immunofluorescence and immunohistochemistry were applied for four candidates (MSN, KRT19, KRT7, JUNB) in both cell lines and tumor xenografts. Results: These experiments demonstrated that KLK4-7 distinctly regulate expression of MSN, KRT19, KRT7 and JUNB on the mRNA and protein levels in ovarian cancer cells and tissues. Protein expression of the top upregulated effectors, MSN and KRT19, was investigated by immunohistochemistry in a cohort of patients (n=66) afflicted with high-grade serous ovarian cancer and related to the immuno-expression levels of KLK4-7. Significant positive associations were found for KRT19/KLK4 (P=0.010), KRT19/KLK5 (P=0.030) and MSN/KLK7 (P=0.001); KRT19 and MSN immuno-expression showed a trend towards significance with KLK6. Conclusions: These findings imply that KLK4-7 exert key modulatory effects on other cancer-related genes and proteins in ovarian cancer. The key downstream effectors of KLK4-7, MSN and KRT19, may represent important therapeutic targets associated with serous ovarian cancer.
2018-12-26 | GSE109261 | GEO
Project description:Colorectal cancer is a leading cause of cancer-related deaths. Mutations in the innate immune receptor AIM2 are frequently identified in patients with colorectal cancer, but how AIM2 modulates colonic tumorigenesis is unknown. Here, we found that Aim2-deficient mice were hypersusceptible to colonic tumor development. Production of inflammasome-associated cytokines and other inflammatory mediators were largely intact in Aim2-deficient mice, however, intestinal stem cells were prone to uncontrolled proliferation. Aberrant Wnt signaling expanded a population of tumor-initiating stem cells in the absence of AIM2. Susceptibility of Aim2-deficient mice to colorectal tumorigenesis was enhanced by a dysbiotic gut microbiota, which was reduced by reciprocal exchange of gut microbiota with wild-type healthy mice. These findings uncover a synergy between a specific host genetic factor and gut microbiota in determining the susceptibility to colorectal cancer. Therapeutic modulation of AIM2 expression and microbiota has the potential to prevent colorectal cancer. We used microarrays to compare the transcriptome Aim2 deficent mice to wild type mice in colon tumor and colitis samples. Here were 12 mice in total, 3 for each genotype and tissue combination.
2015-07-15 | E-GEOD-69436 | biostudies-arrayexpress
Project description:Major depressive disorder is caused by gene-environment interactions and the gut microbiota plays a pivotal role in the development of depression. However, the mechanisms by which the gut microbiota modulates depression remain elusive. Herein, we detected the differentially expressed hippocampal long non-coding RNAs (lncRNAs), messenger RNAs (mRNAs) and microRNAs (miRNAs) between mice inoculated with gut microbiota from major depressive disorder patients or healthy controls, to identify the effects of gut microbiota-dysbiosis on gene regulation patterns at the transcriptome level. We also performed functional analysis to explore the microbial-regulated pathological mechanisms of depression. Two hundred mRNAs, 358 lncRNAs and 4 miRNAs were differentially expressed between the two groups. Functional analysis of these differentially expressed mRNAs indicated dysregulated inflammatory response to be the primary pathological change. Intersecting the differentially expressed mRNAs with targets of differentially expressed miRNAs identified 47 intersected mRNAs, which were mainly related to neurodevelopment. Additionally, we constructed a microbial-regulated lncRNA-miRNA-mRNA network based on RNA-RNA interactions. According to the competitive endogenous RNA hypothesis, two neurodevelopmental ceRNA sub-networks implicating in depression were identified. This study provides new understanding of the pathogenesis of depression induced by gut microbiota-dysbiosis and may act as a theoretical basis for the development of gut microbiota-based antidepressants.
2021-12-31 | GSE189159 | GEO
Project description:Mardinoglu2015 - Tissue-specific genome-scale
metabolic network - Brain medulla
This model is described in the article:
The gut microbiota modulates
host amino acid and glutathione metabolism in mice.
Mardinoglu A, Shoaie S, Bergentall
M, Ghaffari P, Zhang C, Larsson E, Bäckhed F, Nielsen
J.
Mol. Syst. Biol. 2015; 11(10):
834
Abstract:
The gut microbiota has been proposed as an environmental
factor that promotes the progression of metabolic diseases.
Here, we investigated how the gut microbiota modulates the
global metabolic differences in duodenum, jejunum, ileum,
colon, liver, and two white adipose tissue depots obtained from
conventionally raised (CONV-R) and germ-free (GF) mice using
gene expression data and tissue-specific genome-scale metabolic
models (GEMs). We created a generic mouse metabolic reaction
(MMR) GEM, reconstructed 28 tissue-specific GEMs based on
proteomics data, and manually curated GEMs for small intestine,
colon, liver, and adipose tissues. We used these functional
models to determine the global metabolic differences between
CONV-R and GF mice. Based on gene expression data, we found
that the gut microbiota affects the host amino acid (AA)
metabolism, which leads to modifications in glutathione
metabolism. To validate our predictions, we measured the level
of AAs and N-acetylated AAs in the hepatic portal vein of
CONV-R and GF mice. Finally, we simulated the metabolic
differences between the small intestine of the CONV-R and GF
mice accounting for the content of the diet and relative gene
expression differences. Our analyses revealed that the gut
microbiota influences host amino acid and glutathione
metabolism in mice.
This model is hosted on
BioModels Database
and identified by:
MODEL1509220000.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2015-11-03 | MODEL1509220000 | BioModels
Project description:Mardinoglu2015 - Tissue-specific genome-scale
metabolic network - Embryonic tissue
This model is described in the article:
The gut microbiota modulates
host amino acid and glutathione metabolism in mice.
Mardinoglu A, Shoaie S, Bergentall
M, Ghaffari P, Zhang C, Larsson E, Bäckhed F, Nielsen
J.
Mol. Syst. Biol. 2015; 11(10):
834
Abstract:
The gut microbiota has been proposed as an environmental
factor that promotes the progression of metabolic diseases.
Here, we investigated how the gut microbiota modulates the
global metabolic differences in duodenum, jejunum, ileum,
colon, liver, and two white adipose tissue depots obtained from
conventionally raised (CONV-R) and germ-free (GF) mice using
gene expression data and tissue-specific genome-scale metabolic
models (GEMs). We created a generic mouse metabolic reaction
(MMR) GEM, reconstructed 28 tissue-specific GEMs based on
proteomics data, and manually curated GEMs for small intestine,
colon, liver, and adipose tissues. We used these functional
models to determine the global metabolic differences between
CONV-R and GF mice. Based on gene expression data, we found
that the gut microbiota affects the host amino acid (AA)
metabolism, which leads to modifications in glutathione
metabolism. To validate our predictions, we measured the level
of AAs and N-acetylated AAs in the hepatic portal vein of
CONV-R and GF mice. Finally, we simulated the metabolic
differences between the small intestine of the CONV-R and GF
mice accounting for the content of the diet and relative gene
expression differences. Our analyses revealed that the gut
microbiota influences host amino acid and glutathione
metabolism in mice.
This model is hosted on
BioModels Database
and identified by:
MODEL1509220001.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2015-11-03 | MODEL1509220001 | BioModels
Project description:Mardinoglu2015 - Tissue-specific genome-scale
metabolic network - Cerebellum
This model is described in the article:
The gut microbiota modulates
host amino acid and glutathione metabolism in mice.
Mardinoglu A, Shoaie S, Bergentall
M, Ghaffari P, Zhang C, Larsson E, Bäckhed F, Nielsen
J.
Mol. Syst. Biol. 2015; 11(10):
834
Abstract:
The gut microbiota has been proposed as an environmental
factor that promotes the progression of metabolic diseases.
Here, we investigated how the gut microbiota modulates the
global metabolic differences in duodenum, jejunum, ileum,
colon, liver, and two white adipose tissue depots obtained from
conventionally raised (CONV-R) and germ-free (GF) mice using
gene expression data and tissue-specific genome-scale metabolic
models (GEMs). We created a generic mouse metabolic reaction
(MMR) GEM, reconstructed 28 tissue-specific GEMs based on
proteomics data, and manually curated GEMs for small intestine,
colon, liver, and adipose tissues. We used these functional
models to determine the global metabolic differences between
CONV-R and GF mice. Based on gene expression data, we found
that the gut microbiota affects the host amino acid (AA)
metabolism, which leads to modifications in glutathione
metabolism. To validate our predictions, we measured the level
of AAs and N-acetylated AAs in the hepatic portal vein of
CONV-R and GF mice. Finally, we simulated the metabolic
differences between the small intestine of the CONV-R and GF
mice accounting for the content of the diet and relative gene
expression differences. Our analyses revealed that the gut
microbiota influences host amino acid and glutathione
metabolism in mice.
This model is hosted on
BioModels Database
and identified by:
MODEL1509220002.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2015-11-03 | MODEL1509220002 | BioModels
Project description:Mardinoglu2015 - Tissue-specific genome-scale
metabolic network - Brown fat
This model is described in the article:
The gut microbiota modulates
host amino acid and glutathione metabolism in mice.
Mardinoglu A, Shoaie S, Bergentall
M, Ghaffari P, Zhang C, Larsson E, Bäckhed F, Nielsen
J.
Mol. Syst. Biol. 2015; 11(10):
834
Abstract:
The gut microbiota has been proposed as an environmental
factor that promotes the progression of metabolic diseases.
Here, we investigated how the gut microbiota modulates the
global metabolic differences in duodenum, jejunum, ileum,
colon, liver, and two white adipose tissue depots obtained from
conventionally raised (CONV-R) and germ-free (GF) mice using
gene expression data and tissue-specific genome-scale metabolic
models (GEMs). We created a generic mouse metabolic reaction
(MMR) GEM, reconstructed 28 tissue-specific GEMs based on
proteomics data, and manually curated GEMs for small intestine,
colon, liver, and adipose tissues. We used these functional
models to determine the global metabolic differences between
CONV-R and GF mice. Based on gene expression data, we found
that the gut microbiota affects the host amino acid (AA)
metabolism, which leads to modifications in glutathione
metabolism. To validate our predictions, we measured the level
of AAs and N-acetylated AAs in the hepatic portal vein of
CONV-R and GF mice. Finally, we simulated the metabolic
differences between the small intestine of the CONV-R and GF
mice accounting for the content of the diet and relative gene
expression differences. Our analyses revealed that the gut
microbiota influences host amino acid and glutathione
metabolism in mice.
This model is hosted on
BioModels Database
and identified by:
MODEL1509220006.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2015-11-03 | MODEL1509220006 | BioModels