Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA279864 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To confirm the mechanism of miR-29a in liver fibrosis healing, we have employed whole genome microarray expression profiling as a discovery platform to identify genes. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been observed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis. We can get only one gene (PDGF-c) as a target of miR-29a which relate to liver fibrosis and down-regulated more than 1.5 times in common miR-29a injected group than N.C group. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been obserbed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis.
2015-03-31 | E-GEOD-67423 | biostudies-arrayexpress
Project description:To confirm the mechanism of miR-29a in liver fibrosis healing, we have employed whole genome microarray expression profiling as a discovery platform to identify genes. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been observed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis. We can get only one gene (PDGF-c) as a target of miR-29a which relate to liver fibrosis and down-regulated more than 1.5 times in common miR-29a injected group than N.C group.
2015-03-31 | GSE67423 | GEO
Project description:Visual cortical circuits show profound plasticity during early life and are later stabilized by molecular "brakes" limiting excessive circuit rewiring beyond a critical period. How the appearance of these factors is coordinated during the transition from development to adulthood remains unknown. We analyzed the role of miR-29a, a miRNA targeting factors involved in several important pathways for plasticity such as extracellular matrix and chromatin regulation. We found that visual cortical miR-29a expression in the visual cortex dramatically increases with age, but it is not experience-dependent. Precocious high levels of miR-29a induced by targeted intracortical injections of a miR-29a mimic blocked ocular dominance plasticity and caused an early appearance of perineuronal nets. Conversely, inhibition of miR-29a in adult mice using LNA antagomirs activated ocular dominance plasticity, reduced perineuronal net intensity and number, and changed their chemical composition restoring permissive low chondroitin 4-O-sulfation levels characteristic of juvenile mice. Activated adult plasticity had the typical functional and proteomic signature of juvenile plasticity. Transcriptomic and proteomic studies indicated that miR-29a manipulation regulates the expression of plasticity factors acting at different cellular levels, from chromatin regulation to synaptic organization and extracellular matrix remodeling. Intriguingly, the projection of miR-29a regulated gene dataset onto cell-specific transcriptomes revealed that parvalbumin-positive interneurons and oligodendrocytes were the most affected cells. Overall, miR29a is a master regulator of the age-dependent plasticity brakes promoting stability of visual cortical circuits.
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Project description:Visual cortical circuits show profound plasticity during early life and are later stabilized by molecular "brakes" limiting excessive circuit rewiring beyond a critical period. How the appearance of these factors is coordinated during the transition from development to adulthood remains unknown. We analyzed the role of miR-29a, a miRNA targeting factors involved in several important pathways for plasticity such as extracellular matrix and chromatin regulation. We found that visual cortical miR-29a expression in the visual cortex dramatically increases with age, but it is not experience-dependent. Precocious high levels of miR-29a induced by targeted intracortical injections of a miR-29a mimic blocked ocular dominance plasticity and caused an early appearance of perineuronal nets. Conversely, inhibition of miR-29a in adult mice using LNA antagomirs activated ocular dominance plasticity, reduced perineuronal net intensity and number, and changed their chemical composition restoring permissive low chondroitin 4-O-sulfation levels characteristic of juvenile mice. Activated adult plasticity had the typical functional and proteomic signature of juvenile plasticity. Transcriptomic and proteomic studies indicated that miR-29a manipulation regulates the expression of plasticity factors acting at different cellular levels, from chromatin regulation to synaptic organization and extracellular matrix remodeling. Intriguingly, the projection of miR-29a regulated gene dataset onto cell-specific transcriptomes revealed that parvalbumin-positive interneurons and oligodendrocytes were the most affected cells. Overall, miR29a is a master regulator of the age-dependent plasticity brakes promoting stability of visual cortical circuits.
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Project description: Not available
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Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
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Project description:Chronic liver inflammation and fibrosis are central to liver diseases, including the most prevalent metabolic-dysfunction-associated steatohepatitis (MASH), chronic autoimmune liver diseases and liver cancer. However, the mechanism orchestrating the co-occurrence of liver inflammation and fibrosis, both tightly associated with liver diseases, remains elusive. Here, we show that the hepatocyte derived, miR-122 regulates both, liver inflammation and fibrosis, through independent pathways, and that miR-122 is involved in tuning innate and adaptive hepatic immune responses. In parallel, we show that decrease of miR-122 is associated with liver fibrosis in advance or together with liver inflammation. We show that miR-122 regulates liver tolerance, and its absence attenuates bacterial and parasitic infections, and thus functions as a liver immune rheostat. As such, miR-122 presents a therapeutic target.
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Project description:Chronic liver inflammation and fibrosis are central to liver diseases, including the most prevalent metabolic-dysfunction-associated steatohepatitis (MASH), chronic autoimmune liver diseases and liver cancer. However, the mechanism orchestrating the co-occurrence of liver inflammation and fibrosis, both tightly associated with liver diseases, remains elusive. Here, we show that the hepatocyte derived, miR-122 regulates both, liver inflammation and fibrosis, through independent pathways, and that miR-122 is involved in tuning innate and adaptive hepatic immune responses. In parallel, we show that decrease of miR-122 is associated with liver fibrosis in advance or together with liver inflammation. We show that miR-122 regulates liver tolerance, and its absence attenuates bacterial and parasitic infections, and thus functions as a liver immune rheostat. As such, miR-122 presents a therapeutic target.
2025-10-31 | GSE278822 | GEO
Project description:Chronic liver inflammation and fibrosis are central to liver diseases, including the most prevalent metabolic-dysfunction-associated steatohepatitis (MASH), chronic autoimmune liver diseases and liver cancer. However, the mechanism orchestrating the co-occurrence of liver inflammation and fibrosis, both tightly associated with liver diseases, remains elusive. Here, we show that the hepatocyte derived, miR-122 regulates both, liver inflammation and fibrosis, through independent pathways, and that miR-122 is involved in tuning innate and adaptive hepatic immune responses. In parallel, we show that decrease of miR-122 is associated with liver fibrosis in advance or together with liver inflammation. We show that miR-122 regulates liver tolerance, and its absence attenuates bacterial and parasitic infections, and thus functions as a liver immune rheostat. As such, miR-122 presents a therapeutic target.
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