Mitochondrial regulation of bone homeostasis via mitochondria transfer [RNA-seq]
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ABSTRACT:
PROVIDER: PRJNA935661 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23495073_1.fastq.gz | Fastqsanger.gz | |||
| SRR23495073_2.fastq.gz | Fastqsanger.gz | |||
| SRR23495074_1.fastq.gz | Fastqsanger.gz | |||
| SRR23495074_2.fastq.gz | Fastqsanger.gz | |||
| SRR23495075_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Mitochondrial regulation of bone homeostasis via mitochondria transfer
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Project description:Mitochondrial regulation of bone homeostasis via mitochondria transfer [II]
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Project description:To reveal an unappreciated mechanism of mitochondrial regulation of skeletal metabolic homeostasis via mitochondria transfer and provide new insights of the mechanism of glucocorticoid-induced osteoporosis progression.
2024-04-08 | GSE222961 | GEO
Project description:To reveal an unappreciated mechanism of mitochondrial regulation of skeletal metabolic homeostasis via mitochondria transfer and provide new insights of the mechanism of glucocorticoid-induced osteoporosis progression.
2024-04-08 | GSE248687 | GEO
Project description:Recent studies have demonstrated that mitochondria can be transferred between different cell types to control metabolic homeostasis. However, whether the mitochondria transfer network occurred in the skeletal system or regulate skeletal metabolic homeostasis in vivo is not fully elucidated. Herein, we found that osteolineage cells transfer mitochondria to CD11b+ myeloid, B220+ lymphoid and hematopoietic stem and progenitor cells (HSPCs), of which monocytes/macrophages received the most transferred mitochondria. This process was inhibited by GC treatment contributing to the progression of glucocorticoid-induced osteoporosis (GIOP). Further analysis demonstrated that osteolineage cells transfer mitochondria to osteoclastic lineage cells via Miro1 mediated direct contact, and altered the glutathione metabolism, leading to the ferroptosis of osteoclastic lineage cells, thus inhibiting osteoclast activities. These findings revealed an unappreciated mechanism of mitochondrial regulation of skeletal metabolic homeostasis via mitochondria transfer and provide new insights of the mechanism of GIOP progression.
2024-04-08 | GSE225414 | GEO
Project description:It has been reported that human mesenchymal stem cells (MSCs) can transfer mitochondria to the cells with severely compromised mitochondrial function. We tested whether MSCs transfer mitochondria to the cells under several different conditions of mitochondrial dysfunction, including human pathogenic mitochondrial DNA (mtDNA) mutations. Using biochemical selection methods, we found that exponentially growing cells in restrictive media (uridine and bromodeoxyuridine [BrdU]+) after coculture of MSCs (uridine-independent and BrdU-sensitive) and 143B-derived cells with severe mitochondrial dysfunction induced by either long-term ethidium bromide treatment or short-term rhodamine 6G (R6G) treatment (uridine-dependent but BrdU-resistant). The exponentially growing cells had nuclear DNA fingerprint patterns identical to 143B, and a sequence of mtDNA identical to the MSCs. Since R6G causes rapid and irreversible damage to mitochondria without the removal of mtDNA, the mitochondrial function appears to be restored through a direct transfer of mitochondria rather than mtDNA alone. Conditioned media, which were prepared by treating mtDNA-less 143B 0 cells under uridine-free condition, induced increased chemotaxis in MSC, which was also supported by transcriptome analysis. A chemotaxis inhibitory agent blocked mitochondrial transfer phenomenon in the above condition. However, we could not find any evidence of mitochondrial transfer to the cells harboring human pathogenic mtDNA mutations (A3243G mutation or 4,977 bp deletion). Thus, the mitochondrial transfer is limited to the condition of a near total absence of mitochondrial function. Elucidation of the mechanism of mitochondrial transfer will help us create a potential “cell therapy-based mitochondrial restoration or mitochondrial gene therapy” for human diseases caused by mitochondrial dysfunction. time series
2011-11-22 | E-GEOD-33831 | biostudies-arrayexpress
Project description:Mitochondria are the powerhouse of eukaryotic cells, which regulate cell metabolism and differentiation. Recently, mitochondrial transfer between cells has been shown to direct recipient cell fate. However, it is unclear whether mitochondria can translocate to stem cells and whether this transfer alters stem cell fate. Here, we examined mesenchymal stem cell (MSC) regulation by macrophages in the bone marrow environment. We found that macrophages promote osteogenic differentiation of MSCs by delivering mitochondria to MSCs. However, under osteoporotic conditions, macrophages with altered phenotypes and metabolic statuses release oxidatively damaged mitochondria. The transfer of dysfunctional mitochondria to MSCs triggers a reactive oxygen species burst, which leads to metabolic remodeling. We showed that abnormal metabolism in MSCs is caused by the abnormal succinate accumulation, which is a key factor in abnormal osteogenic differentiation. These results reveal that mitochondrial transfer from macrophages to MSCs allows metabolic crosstalk to regulate bone homeostasis. This mechanism identifies a potential target for the treatment of osteoporosis.
2022-09-11 | GSE198806 | GEO
Project description:Intercellular mitochondrial transfer has recently been discovered as a strategy for local microenvironment regulation and repair. However, improving the efficiency of mitochondrial transfer and reducing immune rejection caused by implants is challenging for its application in bone regeneration tissue engineering. We found that bone marrow mesenchymal stem cells (BMSC)s can obtain mitochondria from macrophages through tunnel nanotubes (TNT)s. Mitochondria are crucial for the metabolism and function of BMSC. We further designed a composite hydrogel based on aldehyde sodium hyaluronate and chitosan as the network matrix, containing anti-inflammatory dimethyl itaconate (DMI) and macrophage-targeted zwitterionic nanoparticles (MDVNPs). The acidic bone injury microenvironment triggers a reversible Schiff base reaction in response to pH; further, the released DMI upregulates the M2 phenotype of macrophages by reducing the ROS level. Subsequently, MDVNPs with targeting, high transfection, and low immunogenicity accelerated the efficiency of mitochondrial transfer between macrophages and BMSC by increasing the expression of the mitochondrial transfer regulatory protein Rho GTPase 1 (Miro1). In vitro studies have confirmed that promoting mitochondrial transfer can effectively increase adenosine triphosphate (ATP) and oxidative phosphorylation (OXPHOS) levels in BMSC, promoting osteoblastic differentiation. In the mouse model of critical defect, the composite hydrogel (Gel@MDI) can reduce inflammatory reactions, improve energy metabolism, and enhance bone repair by promoting the balance between the immune system and bone metabolism. This study establishes a potential method for the immune microenvironment to enhance cellular mitochondrial bioenergy and achieve tissue regeneration by regulating mitochondrial transfer between cells.
2024-12-01 | GSE239590 | GEO
Project description:Biomaterial-based bone tissue engineering offers a promising prospect for the treatment of bone defects. In particular, the ability of biomaterials to regulate the immune microenvironment of the defect site is essential for effective bone regeneration. Electro-biomaterials have been confirmed to induce macrophage M2 polarization through metabolic pathways, thereby enhancing bone regeneration. Considering the central role of mitochondria in cellular metabolism and their ability to influence the function of neighboring cells through intercellular transfer, and inspired by the fact that tumor cells can uptake mitochondria from immune cells to generate energy, we hypothesize that the metabolic activation of immune cells by electro-materials can be transmitted to preosteoblasts through mitochondria to promote bone repair. Therefore, this study proposed a conductive micro-hydrogel (CMH) system composed of conductive hydrogel microspheres made from GelMA and poly(3,4-ethylenedioxythiophene):poly(styrenesulfonate) (PEDOT:PSS), which served as scaffolds for defect filling, and a biomimetic periosteum made from poly-l-lactic acid (PLLA) and polydopamine (PDA) for microsphere immobilization and isolation of soft tissue. The microspheres exhibited excellent tissue support and degradation properties, their high specific surface area enhanced tissue remodeling, and their good conductivity eliminated free radicals and induced macrophage M2 polarization, which were confirmed by tests of mechanical property, swelling and degradation, conductivity and assays of cellular biocompatibility, ROS generation, and macrophage phenotype. In vivo experiments using a rat mandibular defect model confirmed the excellent bone repair capabilities of the CMH system, and transcriptomics, metabolomics, and metabolic testing revealed that the CMH system upregulated the oxidative phosphorylation pathway of macrophage, enhancing mitochondrial respiration and ATP production. Mitochondrial tracing experiments demonstrated the transfer of macrophage mitochondria to preosteoblasts, resulting in enhanced metabolic activity and osteogenic differentiation of preosteoblasts. This study may be the first suggest that conductive biomaterials facilitate osteogenic immunomodulation through mitochondrial transfer, which provides a promising method for regulating the immune microenvironment and reveals a novel pathway by which M2 macrophages enhance osteogenesis.
2024-08-11 | GSE274088 | GEO
Project description:It has been reported that human mesenchymal stem cells (MSCs) can transfer mitochondria to the cells with severely compromised mitochondrial function. We tested whether MSCs transfer mitochondria to the cells under several different conditions of mitochondrial dysfunction, including human pathogenic mitochondrial DNA (mtDNA) mutations. Using biochemical selection methods, we found that exponentially growing cells in restrictive media (uridine- and bromodeoxyuridine [BrdU]+) after coculture of MSCs (uridine-independent and BrdU-sensitive) and 143B-derived cells with severe mitochondrial dysfunction induced by either long-term ethidium bromide treatment or short-term rhodamine 6G (R6G) treatment (uridine-dependent but BrdU-resistant). The exponentially growing cells had nuclear DNA fingerprint patterns identical to 143B, and a sequence of mtDNA identical to the MSCs. Since R6G causes rapid and irreversible damage to mitochondria without the removal of mtDNA, the mitochondrial function appears to be restored through a direct transfer of mitochondria rather than mtDNA alone. Conditioned media, which were prepared by treating mtDNA-less 143B rho0 cells under uridine-free condition, induced increased chemotaxis in MSC, which was also supported by transcriptome analysis. A chemotaxis inhibitory agent blocked mitochondrial transfer phenomenon in the above condition. However, we could not find any evidence of mitochondrial transfer to the cells harboring human pathogenic mtDNA mutations (A3243G mutation or 4,977 bp deletion). Thus, the mitochondrial transfer is limited to the condition of a near total absence of mitochondrial function. Elucidation of the mechanism of mitochondrial transfer will help us create a potential “cell therapy-based mitochondrial restoration or mitochondrial gene therapy” for human diseases caused by mitochondrial dysfunction.
2011-11-22 | GSE33831 | GEO