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OPA1 mice gut micobiome

ABSTRACT: OPA1 mice gut micobiome

PROVIDER: PRJEB83275 | ENA |

REPOSITORIES: ENA

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			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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Bulk RNA-Sequencing of brain hemispheres of mice with colitis induced by intestinal epithelial-specific Opa1 deletion

Project description:Whole right brain hemispheres of mice with colitis caused by induced, intestinal epithelial-specific Opa1 knock-out to study the impact of gut inflammation on the brain

2026-01-01 | E-MTAB-15483 | biostudies-arrayexpress

Bulk RNA-sequencing of defined brain regions of mice with chronic DSS-induced colitis and colitis induced bz intestinal epithelial-specific Opa1 deletion

Project description:Selected brain regions of mice with chronic DSS colitis and controls, and mice with colitis caused by induced, intestinal epithelial-specific Opa1 knock-out to study the impact of gut inflammation on the brain

2026-01-01 | E-MTAB-15488 | biostudies-arrayexpress

Gene expression analysis of the cochlea of Opa1 KO mice

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

The loss of OPA1 accelerates intervertebral disc degeneration and osteoarthritis in aged mice

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

The impact of conditional Opa1 Knockout in neural stem cells on transcriptome changes

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

Heart proteome in Cox10 depending on Opa1 processing

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

Optic Atrophy 1 (OPA1) overexpression promotes dyslipidemia and atherosclerosis coupled to altered aortic VSMC function in LDL-R deficient mice

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

The impact of conditional Opa1 Knockout on gene expression profile at single cell level during adult neurogenesis in the hippocampus

2024-06-17 | GSE233461 | GEO

Optic Atrophy 1 (OPA1) overexpression promotes dyslipidemia and atherosclerosis coupled to altered aortic VSMC function in LDL-R deficient mice.

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

Transcriptome analysis in brown adipose tissue of mice lacking the mitochondrial protein optic atrophy 1 (OPA1) in thermogenic adipocytes

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