Ontology highlight
ABSTRACT:
PROVIDER: PRJNA941811 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23724377_1.fastq.gz | Fastqsanger.gz | |||
| SRR23724377_2.fastq.gz | Fastqsanger.gz | |||
| SRR23724378_1.fastq.gz | Fastqsanger.gz | |||
| SRR23724378_2.fastq.gz | Fastqsanger.gz | |||
| SRR23724379_1.fastq.gz | Fastqsanger.gz |
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Project description:Gene expression profiling reveals a potential role of Luteolin in LPS induced depression model LPS depression induced mice were orally treated with luteolin (10 mg/kg body weight) once per day during 8 consecutive days. Microarray gene expression was conducted for isolated mice Neural Stem Cells (NSCs) . Two mice brain were used for each expermient. The Microarray gene expression was conducted on NSCs and hipocampus from LPS depression induced depression mice (LPS group), LPS depression induced depression mice treated with luteolin(LPS+L group), Normal mice (PBS group) and Normal mice treated with luteolin (PBS+L).
2021-11-24 | GSE181522 | GEO
Project description:Gene expression profiling reveals a potential role of Luteolin in LPS induced depression model LPS depression induced mice were orally treated with luteolin (10 mg/kg body weight) once per day during 8 consecutive days. Microarray gene expression was conducted on mice hippocampal tissues. Two mice brains were used for each expermient . The Microarray gene expression was conducted on hipocampus from LPS depression induced mice model(LPS group), LPS depression induced mice model treated with luteolin(LPS+L group), Normal mice (PBS group) and Normal mice treated with luteolin (PBS+L).
2021-11-24 | GSE181285 | GEO
Project description:The distinctive color of brown adipose tissue (BAT) is attributed to its high content of heme-rich mitochondria. Despite this, the mechanisms by which BAT regulates intracellular heme levels remain largely unexplored. Here, we demonstrate that heme biosynthesis is the primary source of heme in brown adipocytes. Inhibiting heme biosynthesis results in an accumulation of the branched-chain amino acids (BCAAs) valine and isoleucine, due to a heme-associated metabolon that channels BCAA-derived carbons into heme biosynthesis. Heme synthesis-deficient brown adipocytes display reduced mitochondrial respiration and lower UCP1 levels compared to wild-type cells. While exogenous heme supplementation can restore intracellular heme levels and mitochondrial function, UCP1 downregulation persists. This sustained UCP1 suppression is linked to epigenetic regulation induced by the accumulation of propionyl-CoA, a byproduct of disrupted heme synthesis. Finally, disruption of heme biosynthesis in BAT impairs thermogenic response and, in female, but not male, mice, hinders the cold- induced clearance of circulating BCAAs in a sex-hormone-dependent manner. These findings establish adipose heme biosynthesis as a key regulator of thermogenesis and sex-dependent BCAA homeostasis.
2025-02-18 | GSE289295 | GEO
Project description:Acute intermittent porphyria (AIP) is an autosomal dominant inborn error of heme biosynthesis due to a pathogenic mutation in the Hmbs gene, resulting in half-normal activity of hydroxymethylbilane synthase. Factors that induce hepatic heme biosynthesis induce episodic attacks in heterozygous patients. The clinical presentation of acute attacks involves the signature neurovisceral pain and may include psychiatric symptoms. Here we used a knock-in mouse line that is biallelic for the Hmbs c.500G>A (p.R167Q) mutation with ~5% of normal hydroxymethylbilane synthase activity to unravel the consequences of severe HMBS deficiency on affective behavior and brain physiology. Hmbs knock-in mice (KI mice) model the rare homozygous dominant form of AIP and were used as tool to elucidate the hitherto unknown pathophysiology of the behavioral manifestations of the disease and its neural underpinnings. Extensive behavioral analyses revealed a selective depression-like phenotype in Hmbs KI mice; transcriptomic and immunohistochemical analyses demonstrated aberrant myelination. The uncovered compromised mitochondrial function in the hippocampus of knock-in mice and its ensuing neurogenic and neuroplastic deficits lead us to propose a mechanistic role for disrupted mitochondrial energy production in the pathogenesis of the behavioral consequences of severe HMBS deficiency and its neuropathological sequelae in the brain.
2020-03-03 | GSE146212 | GEO
Project description:Background: As pain persists, it is often accompanied by the development of negative emotional states, such as depression. Approximately 50%-85% of patients with chronic pain experience depressive symptoms. Ventral tegmental area (VTA) γ--aminobutyric acid (GABA) neurons play a crucial role in regulating emotions. VTA GABA neurons can be mainly classified into those expressing somatostatin (SST) and parvalbumin (PV) neurons. The subtypes of VTA GABA neurons exhibit significant heterogeneity, but it remains unclear whether these subtypes mediate different functions in the development of chronic pain and depression. Inward rectifying potassium channel 4.1 (Kir4.1) is an important potassium channel mainly expressed in astrocytes and plays an important role in regulating neural activity. In lipopolysaccharide (LPS)-induced depression, Kir4.1 in lateral habenula (LHb) was upregulated. Lys05 (an inhibitor of Kir4.1) reversed the Kir4.1-driven depression-like phenotype. However, there was no study has reported the changes of Kir4.1 in chronic pain-induced depression or verified the therapeutic effects of Lys05 on it. Methods: We established chronic constriction injury (CCI) model to induce chronic pain in mice, and used the sugar preference test (SPT), tail suspension test (TST), and open field test (OFT) to detect depressive behavior in mice. Lys05 was injected to investigate the effect of Kir4.1 inhibitors on depression caused by chronic neuropathic pain. The adeno-associated virus (AAV) was designed to knockdown or overexpress the expression of Kir4.1 in VTA astrocytes. Using optogenetic manipulations and transgenic mice, specific activation of VTA GABASST neurons or VTA GABAPV neurons was used to explore which types of VTA GABA neurons Kir4.1 has effects on. Patch-clamp recording was applied to explore the effects of Kir4.1 on the excitability of different types of VTA neurons. Results: Lys05 could reverse the depressive behaviors induced by LPS. In detail, mice treated with 10 mg/kg Lys05 showed increased sucrose preference, decreased immobility durations in TST and increased percent center time in OFT. However, Lys05 didn’t show any specific response to depression behavior in CCI-induced depression mice. Then we found Kir4.1 expression decreased in VTA and LHb of CCI-induced depression mice. Next, we found knockdown of Kir4.1 in the VTA resulted mice became depression but with no hyperalgesia. Correspondingly, overexpress Kir4.1 in VTA astrocytes could reverse the chronic pain-induced depression like states. In the patch clamp, when knocked down Kir4.1 in VTA astrocytes, the excitability of dopamine neurons decreased, GABASST neurons increased, but GABAPV neurons did not change significantly. Specifically excitable VTA GABASST neurons could cause depression in mice, while excitable GABAPV neurons did not. Conclusion: Chronic pain decreases the expression of Kir4.1 in VTA astrocytes, which activates GABASST neurons and in turns inhibits DA neurons, then leads depression.
2025-12-01 | GSE283479 | GEO
Project description:Previously, we showed that dietary heme injured the colonic surface epithelium and induced hyperproliferation by changing the surface to crypt signaling. In this study we investigated whether bacteria play a role in this changed signaling. Dietary heme increased the Bacteroidetes and decreased the Firmicutes in colonic content. This shift was caused by a selective susceptibility of Gram-positive bacteria to the heme cytotoxic fecal waters, which is not observed for Gram-negative bacteria allowing expansion of the Gram-negative community. The increased amount of Gram-negative bacteria increased LPS exposure to colonocytes, however, there is no appreciable immune response detected in the heme-fed mice. There were no signs of sensing of the bacteria by the mucosa, as changes in TLR signaling were not present. This lack of microbe-host cross talk indicated that the changes in microbiota do not play a causal role in the heme-induced hyperproliferation. Mice received control or heme diet for 14 days, whereafter pooled colon samples were analysed on microarrays.
2013-07-18 | E-GEOD-34253 | biostudies-arrayexpress
Project description:This project evaluates the immune regulating properties of maple syrup extract in spleen samples utilizing an LPS induced peritonitis mouse model.
2023-11-03 | MSV000093293 | MassIVE
Project description:Activation of inflammation is tightly associated with metabolic reprogramming in macrophages. The iron-containing tetrapyrrole heme can induce pro-oxidant and pro-inflammatory effects in murine macrophages, but has been associated with polarization towards an anti-inflammatory phenotype in human macrophages. In the current study, we compared the regulatory responses to heme and the prototypical Toll-like receptor (TLR)4 ligand lipopolysaccharide (LPS) in human and mouse macrophages with a particular focus on alterations of cellular bioenergetics. In human macrophages, bulk RNA-sequencing analysis indicated that heme led to an anti-inflammatory transcriptional profile, whereas LPS induced a classical pro-inflammatory gene response. Co-stimulation of heme with LPS caused opposing regulatory patterns of inflammatory activation and cellular bioenergetics in human and mouse macrophages. Specifically, in LPS-stimulated murine, but not human macrophages, heme led to a marked suppression of oxidative phosphorylation and an up-regulation of glycolysis. The species-specific alterations in cellular bioenergetics and inflammatory responses to heme were critically dependent on the availability of nitric oxide (NO) that is generated in inflammatory mouse, but not human macrophages. Accordingly, studies with an inducible nitric oxide synthase (iNOS) inhibitor in mouse, and a pharmacological NO donor in human macrophages, reveal that NO is responsible for the opposing effects of heme in these cells. Taken together, the current findings indicate that NO is critical for the immunomodulatory role of heme in macrophages.
2024-05-13 | GSE255234 | GEO
Project description:CRISPR/Cas9-mediated ablation of two Alas2 intronic cis-elements in G1E-ER-GATA1 cells strongly reduced GATA-1-induced Alas2 transcription, heme biosynthesis, and GATA-1 regulation of other vital constituents of the erythroid cell transcriptome. Bypassing Alas2 function in Alas2 cis-element-mutant (double mutant) cells by providing its catalytic product 5-aminolevulinic acid (5-ALA) rescued heme biosynthesis and a subset of GATA-1-dependent genetic network. Using the same system, we discovered a GATA-1- and heme-dependent circuit that regulates chromatin accessibility during erythroid maturation.
2018-05-30 | GSE114996 | GEO
Project description:The distinctive color of brown adipose tissue (BAT) is attributed to its high content of heme-rich mitochondria. Despite this, the mechanisms by which BAT regulates intracellular heme levels remain largely unexplored. Here, we demonstrate that heme biosynthesis is the primary source of heme in brown adipocytes. Inhibiting heme biosynthesis results in an accumulation of the branched-chain amino acids (BCAAs) valine and isoleucine, due to a heme-associated metabolon that channels BCAA-derived carbons into heme biosynthesis. Heme synthesis-deficient brown adipocytes display reduced mitochondrial respiration and lower UCP1 levels compared to wild-type cells. While exogenous heme supplementation can restore intracellular heme levels and mitochondrial function, downregulation persists. This sustained UCP1 suppression is linked to epigenetic regulation induced by the accumulation of propionyl-CoA, a byproduct of disrupted heme synthesis. Finally, disruption of heme biosynthesis in BAT impairs thermogenic response and, in female, but not male, mice, hinders the cold- induced clearance of circulating BCAAs in a sex-hormone-dependent manner. These findings establish adipose heme biosynthesis as a key regulator of thermogenesis and sex-dependent BCAA homeostasis.
2025-02-17 | PXD060812 | Pride