OPA1 mice gut micobiome
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB83275 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR14050120_1.fastq.gz | Fastqsanger.gz | |||
| ERR14050120_2.fastq.gz | Fastqsanger.gz | |||
| ERR14050121_1.fastq.gz | Fastqsanger.gz | |||
| ERR14050121_2.fastq.gz | Fastqsanger.gz | |||
| ERR14050122_1.fastq.gz | Fastqsanger.gz |
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Project description:RNA was extracted from dissected cochlea at post-natal day 15, from either Opa1+/- mice of their wild-type littermates.
2024-02-26 | GSE232051 | GEO
Project description:NP cells of the intervertebral disc and articular chondrocytes reside in avascular and hypoxic tissue niches. As a consequence of these environmental constraints the cells are primarily glycolytic in nature and were long thought to have a minimal reliance on mitochondrial function. Recent studies have challenged this long-held view and highlighted the increasingly important role of mitochondria in the physiology of these tissues. However, the foundational understanding of mechanisms governing mitochondrial dynamics and function in these tissues is lacking. We investigated the role of mitochondrial fusion protein OPA1 in maintaining the spine and knee joint health in mice. OPA1 knockdown in NP cells altered mitochondrial size and cristae shape and increased the oxygen consumption rate without affecting ATP synthesis. OPA1 governed the morphology of multiple organelles, including peroxisomes, early endosomes and cis-Golgi and its loss resulted in the dysregulation of NP cell autophagy. Metabolic profiling and 13C-flux analyses revealed TCA cycle anaplerosis and altered metabolism in OPA1-deficient NP cells. Noteworthy, Opa1AcanCreERT2 mice with Opa1 deletion in disc and cartilage showed age-dependent disc degeneration, osteoarthritis, and vertebral osteopenia. Our findings underscore that OPA1 regulation of mitochondrial dynamics and multi-organelle interactions is critical in preserving metabolic homeostasis of disc and cartilage.
2025-04-26 | GSE270889 | GEO
Project description:To investigate the function of Opa1 in the regulation of adult neurogenesis, we created a conditional Opa1-knockout mouse line by cross-breeding Nestin-CreERT2;ROSA26YFP mice with Opa1-Flox mice. Using Tamoxifen, we induced Opa1 knockout on 8-weeks-old Nestin-CreERT2;ROSA26YFP;Opa1-Flox mice. We then sorted YFP-positive cells from the hippocampus using flow cytometry at 10 weeks. RNA was extracted from sorted cells and subjected to next generation sequencing.
2024-06-17 | GSE233464 | GEO
Project description:Mitochondrial fusion and fission accompany adaptive responses to stress and altered metabolic demands. Inner membrane fusion and cristae morphogenesis depends on Optic Atrophy 1 (Opa1), which is expressed in different isoforms and is cleaved from a membrane-bound, long to a soluble, short form. Here, we have analyzed the physiological role of Opa1 isoforms and Opa1 processing by generating mouse lines expressing only one cleavable Opa1 isoform or a non-cleavable variant thereof. Our results show that expression of a single cleavable or non-cleavable Opa1 isoform preserves embryonic development and the health of adult mice. Opa1 processing is dispensable under metabolic and thermal stress, but prolongs lifespan and protects against mitochondrial cardiomyopathy in OXPHOS-deficient Cox10-/- mice. Mechanistically, loss of Opa1 processing disturbs the balance between mitochondrial biogenesis and mitophagy, suppressing cardiac hypertrophic growth in Cox10-/- hearts. Our results highlight the critical regulatory role of Opa1 processing, mitochondrial dynamics and metabolism for cardiac hypertrophy.
2024-08-10 | PXD048804 | Pride
Project description:To investigate the function of Opa1 in the regulation of adult neurogenesis, we created a conditional Opa1-knockout mouse line by cross-breeding Nestin-CreERT2;ROSA26YFP mice with Opa1-Flox mice.
2024-06-17 | GSE233461 | GEO
Project description:OPA1 (Optic Atrophy 1), a mitochondrial inner membrane protein involved in mitochondrial cellular metabolism, energy production, calcium homeostasis, and sterol and bile acids (BAs) synthesis. Mitochondria are plastic organelles continuously undergoing biogenesis, fusion, fission, and mitophagy. On these premises, we tested how the overexpression of OPA1, an inner mitochondrial membrane fusion protein, impacts lipids, lipoprotein metabolism, and atherosclerosis development in LDL-R deficient mice (LDLR KO). Methods: OPA1TG/LDLR KO and OPA1ΔHep /LDLR KO were generated and fed with a Western-type diet (WTD) for 12 weeks. Atherosclerosis development was compared to that of LDLR KO mice. In humans, OPA1 expression was investigated in samples from 78 asymptomatic and symptomatic human subjects within the Carotid Plaque Imaging Project (CPIP). Results: OPA1TG/LDLR KO mice showed a significant increase in plasma cholesterol levels mainly in VLDL and LDL fractions. OPA1TG/LDLR KO display a reduction of unconjugated bile acids and higher percentage of conjugated bile acids leading to an increased lipid adsorption. This phenotype was associated with increased atherosclerosis in the aortic root. OPA1 overexpression affects also vascular smooth muscle cell cellular metabolism, leading to an increase in the synthetic vs the proliferative phenotype. Vice versa, hepatocyte deletion of OPA1 improved systemic lipoprotein metabolism and protected from atherosclerosis. The analysis of human atherosclerotic samples indicated that a higher OPA1 expression in the plaque is associated with a reduced degradation of extracellular matrix as well as the expression of markers of cell migration and differentiation. Conclusion: Mitochondrial fusion mediated by OPA1 plays a key role in atherosclerosis by affecting lipoprotein metabolism as well as vascular smooth muscle cell biology.
2025-10-27 | PXD060450 | Pride
Project description:Aims: Mitochondria are involved in cellular metabolism, energy production, calcium homeostasis, sterol and bile acids (BAs) synthesis. Mitochondria are plastic organelles and continuously undergo biogenesis, fusion, fission and mitophagy. On these premises, we tested how the overexpression of OPA1, an inner mitochondrial membrane fusion protein, impacts lipids, lipoprotein metabolism and atherosclerosis development in LDL-R deficient mice (LDLR KO). Methods: OPA1TG/LDLR KO and OPA1ΔHep /LDLR KO were generated and fed with a Western-type diet (WTD) for 12 weeks. Atherosclerosis development was compared to that of LDLR KO mice. In humans, OPA1 expression was investigated in samples from 78 asymptomatic and symptomatic human subjects within the Carotid Plaque Imaging Project (CPIP). Results: OPA1TG/LDLR KO mice showed a significant increase in plasma cholesterol levels mainly in VLDL and LDL fractions. OPA1TG/LDLR KO display a reduction of unconjugated bile acids and higher percentage of conjugated bile acids leading to an increased lipid adsorption. This phenotype was associated with increased atherosclerosis in the aortic root. OPA1 overexpression affects also vascular smooth muscle cell cellular metabolism, leading to an increase in the synthetic vs the proliferative phenotype. Vice versa, hepatocyte deletion of OPA1 improved systemic lipoprotein metabolism and protected from atherosclerosis. The analysis of human atherosclerotic samples indicated that a higher OPA1 expression in the plaque is associated with a reduced degradation of extracellular matrix as well as the expression of markers of cell migration and differentiation. Conclusion: Mitochondrial fusion mediated by OPA1 plays a key role in atherosclerosis by affecting lipoprotein metabolism as well as vascular smooth muscle cell biology.
2025-10-27 | PXD060456 | Pride
Project description:mRNA expression profiles from interscapular brown adipose (iBAT) tissue of 7-week-old OPA1 BAT KO mice and their WT counterparts.
2023-10-10 | GSE218907 | GEO
Project description:Dysfunctions in mitochondria dynamics and metabolism are common pathological processes associated with Parkinson’s disease (PD). Recently, it was shown that an inherited form of PD and dementia is caused by new mutations in the OPA1 gene, which encodes for a key player of mitochondrial fusion and structure. iPSC-derived neural cells from these patients exhibited severe mitochondrial fragmentation, respiration impairment, ATP deficits and heightened oxidative stress. Reconstitution of normal levels of OPA1 in PD-derived neural cells normalized mitochondria morphology and function. OPA1 mutated neuronal cultures showed reduced survival in vitro. Intriguingly, selective inhibition of necroptosis effectively rescued this survival deficit. Additionally, dampening necroptosis in MPTP treated mice protected from DA neuronal cell loss. This human iPSC-based model captures both the early pathological events in OPA1 mutant neural cells and the beneficial effects of blocking necroptosis, highlighting this cell death process as a promising therapeutic target for PD.
2019-01-16 | GSE109228 | GEO
Project description:Adipose tissue macrophages (ATMs) play an important role in regulating adipose tissue inflammation and metabolic homeostasis. Mitochondria are pivotal hubs for macrophage-mediated inflammation. Here, we observed a negative correlation between macrophage optic atrophy type 1 (OPA1) and obesity in both humans and mice. Myeloid OPA1-deficient mice were susceptible to obesity and related systemic insulin resistance, glucose dysregulation, and hepatic steatosis upon high-fat diet (HFD). This is due to the impairment of M2-like macrophage features and the promotion of pro-inflammatory phenotypes. Mechanically, OPA1 loss resulted in metabolic reprogramming, as evidenced by reduced mitochondrial respiration, increased glycolysis, and elevated mtDNA release. This activated the cGAS-STING-IRF7 pathway in M2 macrophages, inducing anti-inflammatory conversion to a pro-inflammatory state. In contrast, myeloid OPA1 transgenic mice exhibited reduced inflammation and obesity. Collectively, we identified macrophage OPA1 as a novel regulator of immune metabolism. Targeting OPA1 may represent an effective therapeutic strategy against obesity and metabolic disorders.
2025-03-13 | GSE291869 | GEO