Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA116773 | ENA |
REPOSITORIES: ENA
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Project description:Chlorella has been used as a food supplement and has been reported to have health benefits. We used the forced swimming test to investigate the influence of Chlorella intake during muscle stress training in mice. Swimming time was about two-fold longer for the Chlorella intake mice than for the control mice. Microarray analysis revealed that the global expression profile of muscle from the Chlorella intake mice was similar to that for intact (nonswimming) mice rather than to that for control swimming mice. By contrast, oxidoreductase activity and the leukotriene synthesis pathway were repressed in Chlorella intake mice. According to measurement of the cytokine activities of primary cultures of spleen, Th1 cytokines, such as interferon-gM-cM-^CM-;and interleukin-2, and granulocyte colony-stimulating factors, such as MIP-1aM-cM-^CM-; GMCSF, and IP-10, were decreased in control swimming mice, but these cytokines were rescued in the Chlorella intake mice. We suggest that the immune response during muscle training can be repressed by intake of Chlorella. The intact (nonswimming) and control (swimming) groups were fed normal food, and the Chlorella intake (swimming) group was fed food including 0.5% Chlorella powder. After 14days, the total RNA was isolated from muscle and samples was pooled for each group (n = 10 for each group).
2011-01-19 | E-GEOD-15798 | biostudies-arrayexpress
Project description:Chlorella has been used as a food supplement and has been reported to have health benefits. We used the forced swimming test to investigate the influence of Chlorella intake during muscle stress training in mice. Swimming time was about two-fold longer for the Chlorella intake mice than for the control mice. Microarray analysis revealed that the global expression profile of muscle from the Chlorella intake mice was similar to that for intact (nonswimming) mice rather than to that for control swimming mice. By contrast, oxidoreductase activity and the leukotriene synthesis pathway were repressed in Chlorella intake mice. According to measurement of the cytokine activities of primary cultures of spleen, Th1 cytokines, such as interferon-g・and interleukin-2, and granulocyte colony-stimulating factors, such as MIP-1a・ GMCSF, and IP-10, were decreased in control swimming mice, but these cytokines were rescued in the Chlorella intake mice. We suggest that the immune response during muscle training can be repressed by intake of Chlorella.
2011-01-19 | GSE15798 | GEO
Project description:Chlorella has been reported to have various physiological activities, including antiarteriosclerotic, cholesterol-lowering, anti-inflammatory, and immunoregulatory effects. However, there has been no report on the long-term effects of chlorella ingestion on immunity. In the present study, 4- to 10-week-old (young) and 4- to 50-week-old (old) female BALB/c mice were sensitized or not with ovalbumin (OVA), and given basic diet containing chlorella powder at 2% or basic diet alone. The effects of chlorella ingestion on immunity were investigated by measurement of splenic cytokines and immunoglobulin (Ig), analysis of T- and B-cells in the spleen and small intestine by flow cytometry, and analysis of the liver by DNA microarray. Results were compared between the young and old, OVA-sensitized and -nonsensitized, and chlorella and non-chlorella ingestion groups. Production of interferon-γ (IFN-γ) was maintained in the nonsensitized old groups, and ratios of T-helper type 1 (Th1) to T-helper type 2 (Th2) cells were similar in the young and old groups. In addition, overproduction of OVA-specific Igs due to OVA sensitization was strongly suppressed, and significant immunotolerance was exhibited irrespective of age. In addition, suppression of T-cell decreases in the spleen due to aging and suppression of changes in T- and B-cells due to OVA sensitization in the small intestinal lymph were demonstrated on flow cytometric analyses. On DNA microarray analysis, immune-related terms including IL11 and major histocompatibility complex (MHC) class 1 were detected, and expression of genes was shown, which were related to IL1-linked genes and complex involving macrophages from the pathways of cytokines and inflammatory response. In addition, suppressions of declined lipid metabolism and energy production were also suggested. Although how the ingredients in chlorella were involved in these changes is unclear, our findings suggest that prevention of decrease in acquired immunity by aging and induction of strong immunotolerance occurred following chlorella ingestion. The Young Control group and Old Control group were fed normal food, and the Old Chlorella intake group was fed food including 2.0% Chlorella powder. The total RNA was isolated from liver and samples was pooled for each group (n = 6 for each group). A table of normalized log2 ratios (where numerator is sample expression data, and denominator is all sample median data) is linked below as a supplementary file.
2010-11-16 | E-GEOD-19032 | biostudies-arrayexpress
Project description:Diet is believed to be an important mediator of oncogenesis and response to anti-cancer therapies, although, no evidence-based dietary guidelines exist for patients with cancer. Limiting protein intake can suppress tumor growth by both inducing nutrient stress and enhancing anti-tumor immunity. However, little is known about the impact of reducing dietary protein on the efficacy of standard anti-cancer therapies, including chemotherapy. Here, we present evidence that reducing protein intake in mice by 50% essentially stops the growth of established tumors, in parallel with inducing a stress response and DNA damage. Further, a reduced protein diet markedly enhances tumor regression upon treatment with 5-fluorouracil (5-FU), accompanied by elevated apoptosis and suppressed mitosis of tumor cells. Proteomic analysis of tumors from 5-FU treated mice fed control or reduced protein diets revealed marked changes including decreased abundance of proteins that mediate DNA repair and replication in mice given diet with reduced protein. In vitro studies mimicking amino acid changes found in tumors from reduced protein-fed mice revealed that cell viability and proliferation rates were similar irrespective of amino acid levels in medium, following 5-FU treatment. In contrast, cGAS-STING signaling, including transcription of Interferon beta 1, was maximally increased in 5-FU treated cells cultured in modified amino acid medium. These findings correlated with enhanced immune cell influx into tumors from mice fed reduced protein diet following 5-FU administration. Collectively, these findings suggest that reducing dietary protein in cancer patients may enhance the efficacy of chemotherapy, which may be mediated by anti-tumor immunity.
2025-03-07 | PXD052110 | Pride
Project description:Chlorella has been reported to have various physiological activities, including antiarteriosclerotic, cholesterol-lowering, anti-inflammatory, and immunoregulatory effects. However, there has been no report on the long-term effects of chlorella ingestion on immunity. In the present study, 4- to 10-week-old (young) and 4- to 50-week-old (old) female BALB/c mice were sensitized or not with ovalbumin (OVA), and given basic diet containing chlorella powder at 2% or basic diet alone. The effects of chlorella ingestion on immunity were investigated by measurement of splenic cytokines and immunoglobulin (Ig), analysis of T- and B-cells in the spleen and small intestine by flow cytometry, and analysis of the liver by DNA microarray. Results were compared between the young and old, OVA-sensitized and -nonsensitized, and chlorella and non-chlorella ingestion groups. Production of interferon-γ (IFN-γ) was maintained in the nonsensitized old groups, and ratios of T-helper type 1 (Th1) to T-helper type 2 (Th2) cells were similar in the young and old groups. In addition, overproduction of OVA-specific Igs due to OVA sensitization was strongly suppressed, and significant immunotolerance was exhibited irrespective of age. In addition, suppression of T-cell decreases in the spleen due to aging and suppression of changes in T- and B-cells due to OVA sensitization in the small intestinal lymph were demonstrated on flow cytometric analyses. On DNA microarray analysis, immune-related terms including IL11 and major histocompatibility complex (MHC) class 1 were detected, and expression of genes was shown, which were related to IL1-linked genes and complex involving macrophages from the pathways of cytokines and inflammatory response. In addition, suppressions of declined lipid metabolism and energy production were also suggested. Although how the ingredients in chlorella were involved in these changes is unclear, our findings suggest that prevention of decrease in acquired immunity by aging and induction of strong immunotolerance occurred following chlorella ingestion.
2010-11-16 | GSE19032 | GEO
Project description:Stress granules (SGs) assembly in response to various stress, has been demonstrated in the regulation of anti-viral immune response and tumor progression. However, lack of evidence to illustrate the relation between SGs formation and allergic diseases. Applying RNA-seq in primary macrophages from G3bp1f/f and G3bp1mac-/- mice, differential expressed genes were defined.
2024-05-01 | GSE264134 | GEO
Project description:The pivotal role of stress in the precipitation of psychiatric diseases is generally accepted. To further elucidate the underlying molecular mechanisms, gene networks and signalling cascades, we investigated the impact of an acute stressor, forced swimming, on the gene expression profile in the hypothalamic paraventricular nucleus (PVN). We performed this study in C57BL/6J and DBA/2J mice, which are known to differ in their reaction to stress. Mice were exposed to forced swimming as stressor, brains were dissected 4h and 8h after stress, both from stressed and unstressed animals, and the RNA profiles from the PVN were evaluated by microarray analysis. Keywords: time course, treatment response, strain differences
2010-10-20 | GSE20877 | GEO
Project description:Metabolic dysfunction-associated steatohepatitis (MASH) and its progression to hepatocellular carcinoma remain major clinical challenges. Chronic endoplasmic reticulum (ER) stress, induced by sustained high-fat diet (HFD) intake, promotes hepatic inflammation, lipid accumulation, and hepatocellular dysfunction during MASH pathogenesis. While transcriptional responses are well-characterized, the post-transcriptional mechanisms underlying hepatocyte adaptation to chronic ER stress remain poorly understood. Using an integrative approach combining transcriptomics, ribosome profiling, cytoplasmic polyadenylation analysis, and cis-regulatory mapping, we define the post-transcriptional landscape induced by chronic HFD exposure. To delineate the specific role of chronic ER stress, we use a hepatocyte-specific knockout of a key regulator of translational control under prolonged ER stress. We show that ~70% of HFD-induced gene expression changes are modulated at the translational level. A distinct subset of mRNAs - enriched in suboptimal codons and bearing short poly(A) tails under normal diet - becomes selectively activated upon HFD-induced poly(A) tail elongation. These transcripts, associated with cell cycle, immune response, fibrosis, and tissue remodeling, correlate with MASH severity in both murine models and human samples. Their regulation is mediated by cis-elements in the 3' UTR that coordinate polyadenylation and deadenylation. Loss of this adaptive response exacerbates liver damage and tumor burden in HFD-fed mice.
2026-03-05 | E-MTAB-16294 | biostudies-arrayexpress
Project description:Metabolic dysfunction-associated steatohepatitis (MASH) and its progression to hepatocellular carcinoma remain major clinical challenges. Chronic endoplasmic reticulum (ER) stress, induced by sustained high-fat diet (HFD) intake, promotes hepatic inflammation, lipid accumulation, and hepatocellular dysfunction during MASH pathogenesis. While transcriptional responses are well-characterized, the post-transcriptional mechanisms underlying hepatocyte adaptation to chronic ER stress remain poorly understood. Using an integrative approach combining transcriptomics, ribosome profiling, cytoplasmic polyadenylation analysis, and cis-regulatory mapping, we define the post-transcriptional landscape induced by chronic HFD exposure. To delineate the specific role of chronic ER stress, we use a hepatocyte-specific knockout of a key regulator of translational control under prolonged ER stress. We show that ~70% of HFD-induced gene expression changes are modulated at the translational level. A distinct subset of mRNAs - enriched in suboptimal codons and bearing short poly(A) tails under normal diet - becomes selectively activated upon HFD-induced poly(A) tail elongation. These transcripts, associated with cell cycle, immune response, fibrosis, and tissue remodeling, correlate with MASH severity in both murine models and human samples. Their regulation is mediated by cis-elements in the 3'UTR that coordinate polyadenylation and deadenylation. Loss of this adaptive response exacerbates liver damage and tumor burden in HFD-fed mice.
2026-03-05 | E-MTAB-16295 | biostudies-arrayexpress
Project description:Metabolic dysfunction-associated steatohepatitis (MASH) and its progression to hepatocellular carcinoma remain major clinical challenges. Chronic endoplasmic reticulum (ER) stress, induced by sustained high-fat diet (HFD) intake, promotes hepatic inflammation, lipid accumulation, and hepatocellular dysfunction during MASH pathogenesis. While transcriptional responses are well-characterized, the post-transcriptional mechanisms underlying hepatocyte adaptation to chronic ER stress remain poorly understood. Using an integrative approach combining transcriptomics, ribosome profiling, cytoplasmic polyadenylation analysis, and cis-regulatory mapping, we define the post-transcriptional landscape induced by chronic HFD exposure. To delineate the specific role of chronic ER stress, we use a hepatocyte-specific knockout of a key regulator of translational control under prolonged ER stress. We show that ~70% of HFD-induced gene expression changes are modulated at the translational level. A distinct subset of mRNAs - enriched in suboptimal codons and bearing short poly(A) tails under normal diet - becomes selectively activated upon HFD-induced poly(A) tail elongation. These transcripts, associated with cell cycle, immune response, fibrosis, and tissue remodeling, correlate with MASH severity in both murine models and human samples. Their regulation is mediated by cis-elements in the 3' UTR that coordinate polyadenylation and deadenylation. Loss of this adaptive response exacerbates liver damage and tumor burden in HFD-fed mice.
2026-03-05 | E-MTAB-16293 | biostudies-arrayexpress