Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA127745 | ENA |
REPOSITORIES: ENA
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Project description:The mitochondrial protein repertoire varies depending on cellular states, tissue type, species, and disease state. However, little is known about how this repertoire changes under different cellular or disease states. To gain a better understanding of dynamic mitochondrial proteomic changes, we compared alterations of mitochondrial proteome with transcriptome under mitochondrial DNA depletion. Total RNA obtained from 143B TK- osteosarcoma ?+ cells or 143B TK- osteosarcoma ?° cells
2010-07-17 | E-GEOD-22970 | biostudies-arrayexpress
Project description:Analysis of gene expression patterns in 143B osteosarcoma tumors that formed from 143B cells that harbor different background of mtDNA or no mtDNA. The hypothesis tested in this study was that mtDNA genotypes exert influence on chromosomal gene expression.
2016-12-31 | GSE73120 | GEO
Project description:Mitochondria have been implicated in insulin resistance and beta cell dysfunction, both of which comprise the core pathophysiology of type 2 diabetes mellitus (T2DM). It has also recently been found that mtDNA haplogroups are distinctively associated with susceptibility to T2DM at least in Koreans and Japanese. To investigate the functional consequences of different mtDNA, we compared gene expression profiles between cybrid clones harboring three different mtDNA haplogroups (D5, F, and N9a). To produce hybrid clones, we fused mtDNA-depleted osteosarcoma cell line (143B TK- rho0) with nucleus-lacking platelets from twelve donors harboring the three haplogroups.
2012-04-01 | GSE26244 | GEO
Project description:Mitochondria have been implicated in insulin resistance and beta cell dysfunction, both of which comprise the core pathophysiology of type 2 diabetes mellitus (T2DM). It has also recently been found that mtDNA haplogroups are distinctively associated with susceptibility to T2DM at least in Koreans and Japanese. To investigate the functional consequences of different mtDNA, we compared gene expression profiles between cybrid clones harboring three different mtDNA haplogroups (D5, F, and N9a). To produce hybrid clones, we fused mtDNA-depleted osteosarcoma cell line (143B TK- rho0) with nucleus-lacking platelets from twelve donors harboring the three haplogroups. A total of twelve cybrid clones from the three mtDNA haplogroups were obtained: D5 (n=3), F (n=5), and N9a (n=4). For each clone, four technical replicates were obtained and hybridized to the array. For rho0 cell, six technical replicates were obtained and hybridized to the array.
2012-03-31 | E-GEOD-26244 | biostudies-arrayexpress
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:Pulmonary metastasis is the main cause of medical failure and death of osteosarcoma patients. Our recent study identified IRX1 as a potential metastasis-driving gene in osteosarcoma. Studies showed that IRX1 can promote the migration, invasion and anoikis resistance of osteosarcoma cells. We generated 143B stable IRX1 knockdown and control cell lines, and found that IRX1 knockdown can inhibit the pulmonary metastasis of 143B cells in orthotopic mouse osteosarcoma model. Expression microarrays are performed in143B-shCtrl and 143B-shIRX1 cells to study the mechanism of IRX1 on promoting metastasis of osteosarcoma
2015-08-25 | E-GEOD-55958 | biostudies-arrayexpress
Project description:Mitochondria generate signals of adaptation that regulate nuclear genes expression via retrograde signaling. But this phenomenon is complexified when qualitatively different mitochondria and mitochondrial DNA (mtDNA) coexist within cells. Although this cellular state of heteroplasmy leads to divergent phenotypes clinically, its consequences on cellular function and the cellular transcriptome are unknown. To interrogate this phenomenon, we generated somatic cell cybrids harboring increasing levels of a common mtDNA mutation (tRNALeu(UUR) 3243A>G) and mapped the resulting cellular phenotypes and transcriptional profiles across the complete range of heteroplasmy. Small increases in mutant mtDNAs caused relatively modest defect in mitochondrial oxidative capacity, but resulted in sharp transitions in mitochondrial ultrastructure and in the nuclear and mitochondrial transcriptomes, with the critical functional threshold corresponding to the induction of epigenetic regulatory systems. Principal component analysis underscores how each heteroplasmy level occupies a different "transcriptional space", with low levels heteroplasmy (20-30%) producing a dose-response linear progression in one direction, and mutationload of 50, 60 and 90% producing changes in the opposite direction. Hence, subtle changes in mitochondrial energetics can act through the epigenome to generate the phenotypes of the common “complex” diseases. Cells were generated by transferring the wildtype (3243A) and mutant (3243G) mtDNAs from a heteroplasmic 3243A>G patient’s lymphoblastoid cell line into 143B(TK-) mtDNA-deficient (ρo) cells and selected for transmitochondrial cybrids. Subsequent mtDNA depletion, reamplification, and cloning (Wiseman and Attardi, 1978) resulted in a series of stable cybrids harboring approximately 0, 20, 30, 50, 60, 90, and 100% 3243G mutant mtDNAs. Total RNA extracted from each cell line was then extracted, depleted of rRNA, and measured in sequenced in triplicates.
2014-09-02 | E-GEOD-56158 | biostudies-arrayexpress
Project description:Pulmonary metastasis is the main cause of medical failure and death of osteosarcoma patients. Our recent study identified IRX1 as a potential metastasis-driving gene in osteosarcoma. Studies showed that IRX1 can promote the migration, invasion and anoikis resistance of osteosarcoma cells. We generated 143B stable IRX1 knockdown and control cell lines, and found that IRX1 knockdown can inhibit the pulmonary metastasis of 143B cells in orthotopic mouse osteosarcoma model.
2015-08-25 | GSE55958 | GEO
Project description:To identify target genes regulated by ALKBH5 in osteosarcoma, we silenced the expression of ALKBH5 in osteosarcoma cell line-143B and tested its effect on 143B transcriptome.
2022-06-28 | GSE154528 | 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