Mitochondria transfer from immune cells enables lymph node metastasis
Ontology highlight
ABSTRACT:
INSTRUMENT(S): DNBSEQ-T7
ORGANISM(S): Mus musculus
SUBMITTER: Azusa Terasaki
PROVIDER: E-MTAB-16050 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:In a previous study, we found that H2S alleviates salinity stress in cucumber by maintaining the Na+/K+ balance and by regulating H2S metabolism and the oxidative stress response. However, little is known about the molecular mechanisms behind H2S-regulated salt-stress tolerance in cucumber. Here, an integrated transcriptomic and proteomic analysis based on RNA-seq and 2-DE was used to investigate the global mechanism underlying H2S-regulated salt-stress tolerance. In total, 11 761 differentially expressed genes (DEGs) and 61 differentially expressed proteins (DEPs) were identified. Analysis of the pathways associated with the DEGs showed that salt stress enriched expression of genes in primary and energy metabolism, such as photosynthesis, carbon metabolism and biosynthesis of amino acids. Application of H2S significantly decreased these DEGs but enriched DEGs related to plant-pathogen interaction, sulfur-containing metabolism, cell defense and signal transduction pathways. Notably, changes related to sulfur-containing metabolism and cell defense were also observed through proteome analysis, such as Cysteine synthase 1, Glutathione S-transferase U25-like, Protein disulfide-isomerase and Peroxidase 2. We present the first global analysis of the mechanism underlying H2S regulation of salt-stress tolerance in cucumber through tracking changes in the expression of specific proteins and genes.
2021-09-09 | PXD020642 | Pride
Project description:Background: Microorganisms are the major cause of food spoilage during storage, processing and distribution. Pseudomonas fluorescens is a typical spoilage bacterium that contributes to a large extent to the spoilage process of proteinaceous food. RpoS is considered an important global regulator involved in stress survival and virulence in many pathogens. Our previous work revealed that RpoS contributed to the spoilage activities of P. fluorescens by regulating resistance to different stress conditions, extracellular acylated homoserine lactone (AHL) levels, extracellular protease and total volatile basic nitrogen (TVB-N) production. However, RpoS-dependent genes in P. fluorescens remained undefined. Results: RNA-seq transcriptomics analysis combined with quantitative proteomics analysis basing on multiplexed isobaric tandem mass tag (TMT) labeling was performed for the P. fluorescens wild-type strain UK4 and its derivative carrying a rpoS mutation. A total of 375 differentially expressed genes (DEGs) and 212 differentially expressed proteins (DEPs) were identified in these two backgrounds. The DGEs were further verified by qRT-PCR tests, and the genes directly regulated by RpoS were confirmed by 5’-RACE-PCR sequencing. The combining transcriptome and proteome analysis revealed a role of this regulator in several cellular processes, including polysaccharide metabolism, intracellular secretion and extracellular structures, cell well biogenesis, stress responses, ammonia and biogenic amine production, which may contribute to biofilm formation, stress resistance and spoilage activities of P. fluorescens. Moreover, in this work we indeed observed that RpoS contributed to the production of the macrocolony biofilm’s matrix.
2019-11-12 | PXD010845 | Pride
Project description:Rett Syndrome (RTT) is a severe neurological disorder predominantly affecting females, caused by mutations in the methyl CpG binding protein 2 (MECP2) gene. Understanding the pathophysiology of RTT at a cellular and molecular level is crucial for the development of targeted therapies. This project aims to dissect the molecular underpinnings of RTT using a novel in vitro model system based on a commercially available human neural progenitor cell line, ReNCell. We have engineered multiple distinct ReNCell lines to mimic specific genetic alterations associated with RTT, providing a robust platform for mechanistic studies and drug screening. One cell line is a complete knockout of MECP2, serving as a model to investigate the effects of total loss of MeCP2 function. This model helps in understanding the full spectrum of MeCP2's roles in neural development and maintenance, and in identifying compensatory mechanisms that could be targeted therapeutically. The other line involves the knockdown of NEAT1, a long non-coding RNA known to be involved in the pathogenesis of several neurological disorders, including RTT. Recent studies suggest NEAT1 plays a critical role in the neuronal cellular response to MECP2 dysfunction. By reducing NEAT1 expression, we aim to elucidate its contribution to RTT pathology and explore its potential as a therapeutic target. Here we characterize the transcriptome of these cell lines, including the wild type (control), at the progenitor state and after 7 days of differentiation with three replicates each.
2024-11-17 | E-MTAB-14048 | biostudies-arrayexpress
Project description:We performed RNAseq, metabolomics and pathway enrichment analysis on cardiac tissue from naked mole-rats (Heterocephalus glaber) and from seven other members of African mole rat genera, Cape mole-rat (Georychus capensis), Cape dune mole-rat (Bathyergus suillus), Common mole-rat (Cryptomys hottentotus hottentotus), Natal mole-rat (C. h. natalenesis), Mahali mole rat (C. h. mahali), Highveld mole-rat (C. h. pretoriae) and Damaraland mole-rats (Fukomys damarensis) representing differing burrow and soil types, degrees of sociality, lifespan and hypoxia tolerance. In addition, we include the evolutionarily highly divergent hottentot golden mole (Ambysomus hottentotus), an Afrotherian subterranean, solitary mammal, and the C57/BL6 laboratory mouse as a standard mammal control. After RNA sequencing, we removed the reads mapped to rRNAs and get rawdata, then we filtered the low quality reads (More than 20% of the bases qualities are lower than 10), reads with adaptors and reads with unknown bases (N bases more than 5%) to get the clean reads. These are the data uploaded.
2024-02-20 | E-MTAB-13808 | biostudies-arrayexpress
Project description:Retinitis pigmentosa (RP) is a photoreceptor disease that affects approximately 100,000 people in the United States. There are currently very limited treatment options and the prognosis for most patients is progressive vision loss. Unfortunately, the understanding of the molecular underpinnings of RP initiation and progression is still poorly understood. However, the development of animal models of RP, coupled with high-throughput sequencing, has provided an opportunity to study the underlying cellular and molecular changes of this disease. Using RNA-Seq, we present the first retinal transcriptome analysis of the rd10 murine model of retinal degeneration. RNA-Seq on whole-retina samples from rd10, wild-type and GFP-expressing mouse retina. Three biological replicates of each.
2014-10-26 | E-GEOD-56473 | biostudies-arrayexpress
Project description:Transmissible gastroenteritis virus (TGEV) is a member of Coronaviridae family. Our previous research showed that TGEV infection could induce mitochondrial dysfunction and up-regulat miR-222 level. Therefore, we presumed that miR-222 might be implicated in regulating mitochondrial dysfunction induced by TGEV infection. To verify the hypothesis, the effect of miR-222 on mitochondrial dysfunction was detected and showed that miR-222 attenuated TGEV-induced mitochondrial dysfunction. To investigate the underlying molecular mechanism of miR-222 in TGEV-induced mitochondrial dysfunction, a quantitative proteomic analysis of PK-15 cells that were transfected with miR-222 mimics and infected with TGEV was performed. In total, 4151 proteins were quantified and 100 differentially expressed proteins were obtained (57 up-regulated, 43 down-regulated), among which thrombospondin-1 (THBS1) and cluster of differentiation 47 (CD47) were down-regulated. THBS1 was identified as the target of miR-222. Knockdown of THBS1 and CD47 increased mitochondrial Ca2+ level and decreased mitochondrial membrane potential (MMP) level. Together, our data establish a significant role of miR-222 in regulating mitochondrial dysfunction in response to TGEV infection.
2018-12-19 | PXD010927 | Pride
Project description:Transcriptomic analysis of the brown bear (Ursus arctos) tissues during both active and inactive phases has unveiled significant differential gene expression, with thousands of genes exhibiting altered activity in all studied tissues (muscle, liver, adipose...). Nevertheless, transcriptional analyses of hibernating animal tissues are limited to organs that are important in metabolism. No information is available about the variations of gene expression in tissues that may have a lower impact on metabolism, like the skin, which is mainly a support tissue and a mechanical barrier against the external environment. That experiment brings information about the gene expression variations in the bear skin during hibernation.
2025-09-05 | E-MTAB-14479 | biostudies-arrayexpress
Project description:Abstract Isorhynchophylline, a tetracyclic indole alkaloid, has anti-inflammatory and antioxidant activities against cardiovascular diseases and central nervous system disorders. Acute lung injury (ALI) is a manifestation of inflammation concentrated in the lungs and has a high incidence rate and mortality. Here, we established a mouse model of ALI and observed the effects of isorhynchophylline. Proteomic results showed that 5727 proteins were detected in mouse lung tissues, and 16 proteins were screened out. Isorhynchophylline could reverse the trend of these differential proteins. In addition, isorhynchophylline can act on integrin alpha M to reduce neutrophil recruitment and thereby produce anti-inflammatory effects and may suppress neutrophil migration through the leukocyte transendothelial migration pathway. TUNEL and RT-PCR experiments revealed that LPS-induced ALI in mice increases the apoptosis of lung tissues, damage to alveolar epithelial cells and levels of inflammatory factors. Treatment with isorhynchophylline can repair tissues, improve lung tissue pathology and reduce lung inflammation.
2024-06-23 | PXD050432 | Pride
Project description:Cholangiocarcinoma (CCA) is a devastating liver cancer characterized by high aggressiveness and resistance to therapy, which results to poor prognosis. Signals imposed by oncogenic pathways, such as transforming growth factor β (TGFβ) frequently contribute to CCA development. In this study, we explored novel effectors of the TGFβ pathway in CCA by gene expression profiling. We identified the long non-coding RNA LINC00313 as a novel target gene of TGFβ signalling in CCA cells. TGFβ induced LINC00313 expression in a TβRI/Smad-dependent manner. Subcellular fractionation showed that LINC00313 is a predominantly nuclear lncRNA. By integrating RNA-seq and ATAC-seq data from LINC00313 over-expressing cells, we observed that LINC00313 regulates the expression of several genes involved in the Wnt signalling pathway. As a proof of concept, we focused on the gene encoding transcription factor 7 (TCF7), a major effector that drives transcription of Wnt-target genes. LINC00313 gain of function resulted in increased TCF7 expression, while its loss of function diminished basal or TGFβ-induced TCF7 expression levels. Interestingly, LINC00313 enhanced basal or chemically induced TCF/LEF-dependent transcriptional responses, promoted colony-forming capacities of CCA cells in vitro and accelerated tumor growth in vivo. We also report that genes associated with LINC00313 over-expression recapitulate poor prognosis human CCA associated with a reduced overall survival and KRAS mutations. To decipher the underlying molecular functions of LINC00313, we identified its interacting proteins by performing an unbiased RNA pull-down assay followed by mass spectrometry. We demonstrated that actin-like 6A (ACTL6A), a subunit of the SWI/SNF chromatin remodelling complex specifically binds to LINC00313 and impacts TCF7 expression and TCF/LEF signalling output. Thus, we propose a model whereby TGFβ induces LINC00313, in order to regulate the expression of a subset of target genes, such as TCF7 possibly in co-operation with the SWI/SNF chromatin remodelling complex, via establishing direct interaction with ACTL6A. By regulating key genes of the Wnt pathway, LINC00313 fine-tunes Wnt/TCF/LEF-dependent transcriptional responses and boosts cholangiocarcinogenesis.
2024-02-05 | E-MTAB-12030 | biostudies-arrayexpress
Project description:The aim of this study is to identify genes whose expression is under the control of IRE1A and IRE1B during a chronic proteotoxic endoplasmic reticulum stress induced by tunicamycin. The transcriptional response has been measured in separated shoot and root tissues from Arabidopsis seedlings.
2024-02-29 | E-MTAB-12284 | biostudies-arrayexpress