Expression data from glucosamine-treated human synovial MH7A cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE72575 | GEO | 2016/11/07
SECONDARY ACCESSION(S): PRJNA294384
REPOSITORIES: GEO
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Project description:The O-linked β-N-acetylglucosamine (O-GlcNAc) modification on intracellular proteins controls diverse biological processes. Though sustained hyper-O-GlcNAcylation aggravates pathogenesis of many chronic diseases, accumulating evidence also indicates that acute augmentation in O-GlcNAcylation seems to benefit disease healing in some cases. Glucosamine (GlcN) is a freely available and commonly used dietary supplement for human cartilage health, which also activates the hexosamine biosynthesis pathway and induces protein O-GlcNAcylation. Here we show that both GlcN early and late therapies effectively facilitate cardiac recovery in mice by elevating accumulation of Ly6Clow Mo/Mps in infarcted hearts. Eliminating Mo/Mps with clodronate liposomes fully abolishes aforementioned cardiac healing role of GlcN. Importantly, GlcN supplementation accelerates not only in vitro mobility of reparative Mo/Mps but also in vivo infiltration of Ly6Clow Mos. Mechanistically, GlcN positively regulates transcription of myeloid CX3C chemokine receptor 1 (Cx3cr1) by improving STAT1 O-GlcNAcylation, which stabilizes STAT1 and subsequently promotes chemotaxis and infiltration of Ly6Clow Mos. In summary, we identify a novel anti-inflammatory role of GlcN and suggest that its protective effects are mediated through chemotaxis of Ly6Clow Mos in a STAT1/CX3CR1-dependent fashion, which is controlled by O-GlcNAcylation of STAT1. Our study provides a novel clue for Mo/Mps modulator therapies aimed at reducing post-MI hyperinflammation in ischemic myocardium.
2022-04-06 | GSE193613 | GEO
Project description:D-Glucosamine (2-amino-2-deoxy-D-glucose, C.A.S.# 3416-24-8) (GlcN) is a freely available and commonly used dietary supplement possibly promoting cartilage health in humans which also acts as an inhibitor of glycolysis. We here find that GlcN extends C. elegans lifespan by impairing glucose metabolism to activate AMP-activated protein kinase (AMPK/AAK2) leading to increased mitochondrial biogenesis. Consistent with the concept of mitohormesis, this promotes increased formation of mitochondrial reactive oxygen species (ROS) and p38/PMK-1-mediated stress signaling culminating in increased expression of the nematodal amino acid-transporter 1 (aat-1) gene. Ameliorating mitochondrial ROS formation as well as impairment of aat-1-expression abolishes GlcN-mediated lifespan extension in a NRF2/SKN-1-dependent fashion. Notably and unlike other calorie restriction mimetics (CRM) like 2-deoxy-D-glucose (2DG, DOG), GlcN extends lifespan of aging C57BL/6 mice (log-rank: p=0.002; cox regression: p=0.01) similarly paralleled by an induction of mitochondrial biogenesis, increased expression of several murine amino acid transporters, as well as increased amino-acid catabolism. Taken together, GlcN mimics a ketogenic diet to extend healthspan in evolutionary distinct species. 24 samples: 12 mRNA profiles of C.elegans: 6 without GlcN and 6 with GlcN supplementaion; 12 mRNA profiles of M.musculus: 6 without GlcN and 6 with GlcN supplementaion
2014-03-07 | E-GEOD-54853 | biostudies-arrayexpress
Project description:D-Glucosamine (2-amino-2-deoxy-D-glucose, C.A.S.# 3416-24-8) (GlcN) is a freely available and commonly used dietary supplement possibly promoting cartilage health in humans which also acts as an inhibitor of glycolysis. We here find that GlcN extends C. elegans lifespan by impairing glucose metabolism to activate AMP-activated protein kinase (AMPK/AAK2) leading to increased mitochondrial biogenesis. Consistent with the concept of mitohormesis, this promotes increased formation of mitochondrial reactive oxygen species (ROS) and p38/PMK-1-mediated stress signaling culminating in increased expression of the nematodal amino acid-transporter 1 (aat-1) gene. Ameliorating mitochondrial ROS formation as well as impairment of aat-1-expression abolishes GlcN-mediated lifespan extension in a NRF2/SKN-1-dependent fashion. Notably and unlike other calorie restriction mimetics (CRM) like 2-deoxy-D-glucose (2DG, DOG), GlcN extends lifespan of aging C57BL/6 mice (log-rank: p=0.002; cox regression: p=0.01) similarly paralleled by an induction of mitochondrial biogenesis, increased expression of several murine amino acid transporters, as well as increased amino-acid catabolism. Taken together, GlcN mimics a ketogenic diet to extend healthspan in evolutionary distinct species.
2014-03-07 | GSE54853 | GEO
Project description:Amino sugars, particularly glucosamine (GlcN) and N-acetylglucosamine (GlcNAc) are abundant carbon and nitrogen sources that are continually supplied in host secretions and the diet to biofilms colonizing the human mouth. Evidence is emerging that these amino sugars may provide an ecological advantage to beneficial commensals over oral pathobionts. Here we performed transcriptome analysis on Streptococcus mutans and Streptococcus gordonii growing in single-species or dual-species cultures with glucose, GlcN or GlcNAc as the primary carbohydrate source. Compared to glucose, GlcN caused drastic transcriptomic shifts in each bacterium when they were cultured alone. Likewise, co-cultivation in the presence of GlcN yielded transcriptomic profiles that were dramatically different than the single-species results from GlcN-grown cells. In contrast, GlcNAc elicited only minor changes in the transcriptome of either organism, in both single- and dual-species cultures. Interestingly, genes involved in pyruvate metabolism were among the most significantly affected by GlcN in both species, and these changes were consistent with measurements of pyruvate in culture supernates. Differing a previous report, growth of S. mutans alone with GlcN inhibited expression of multiple operons required for mutacin production. Co-cultivation with S. gordonii consistently increased the expression by S. mutans of two manganese transporter operons (slo and mntH) and decreased expression of mutacin genes. Conversely, S. gordonii appeared to be less affected by the presence of S. mutans, but did show increases in genes for biosynthetic processes in the co-cultures. In conclusion, amino sugars profoundly altered the interactions between the pathogen and the commensal, likely by reprogramming their central metabolism.
2020-06-09 | GSE152021 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE3101: Chitin oligosaccharide induction GSE3102: Crab shell attachment GSE3103: Chitin sensor Abstract: Chitin, an insoluble polymer of GlcNAc, is an abundant source of carbon, nitrogen, and energy for marine microorganisms. Microarray expression profiling and mutational studies of Vibrio cholerae growing on a natural chitin surface, or with the soluble chitin oligosaccharides (GlcNAc)(2-6), GlcNAc, or the glucosamine dimer (GlcN)2 identified three sets of differentially regulated genes. We show that (i) ChiS, a sensor histidine kinase, regulates expression of the (GlcNAc)(2-6) gene set, including a (GlcNAc)2 catabolic operon, two extracellular chitinases, a chitoporin, and a PilA-containing type IV pilus, designated ChiRP (chitin-regulated pilus) that confers a significant growth advantage to V. cholerae on a chitin surface; (ii) GlcNAc causes the coordinate expression of genes involved with chitin chemotaxis and adherence and with the transport and assimilation of GlcNAc; (iii) (GlcN)2 induces genes required for the transport and catabolism of nonacetylated chitin residues; and (iv) the constitutively expressed MSHA pilus facilitates adhesion to the chitin surface independent of surface chemistry. Collectively, these results provide a global portrait of a complex, multistage V. cholerae program for the efficient utilization of chitin. Refer to individual Series
2006-03-07 | E-GEOD-4388 | biostudies-arrayexpress
Project description:Streptomycetes are saprophytic bacteria that grow on complex polysaccharides, such as cellulose, starch, chitin and chitosan. For the monomeric building blocks glucose, maltose and N-acetylglucosamine the metabolic pathway is well documented, but that of glucosamine (GlcN) is currently unknown. Importantly, GlcN is lethal to Streptomyces coelicolor nagB mutants, which lack glucosamine-6-phosphate deaminase activity. Here we report that spontaneous and directed mutations in the gene for the ROK-family protein RokL6 (SCO1447) relieve GlcN toxicity in nagB mutants of S. coelicolor. RNA sequencing, ChIP-Seq and over-expression studies revealed that RokL6 acts by directly repressing SCO1448, which encodes a sugar exporter; RokL6 thereby only binds to the rokL6-SCO1448 intergenic region in vivo, with consensus binding site C(T)TATCAGG - 7 nt - CCTGATAG(A). The exact transcriptional start sites for rokL6 and SCO1448 were determined using 5’RACE. RokL6 represses the transcription of both rokL6 and SCO1448 by binding to overlapping promoter sequences. Taken together, our data show that RokL6 and SCO1448 are novel GlcN-related genes, whereby RokL6 directly controls the transcription of SCO1448. The latter is a key protein in the defense of S. coelicolor against the toxicity of GlcN in a nagB-mutant background, most likely via the export of GlcN-derived toxic intermediates.
2023-06-19 | GSE234438 | GEO
Project description:Streptomycetes are saprophytic bacteria that grow on complex polysaccharides, such as cellulose, starch, chitin and chitosan. For the monomeric building blocks glucose, maltose and N-acetylglucosamine the metabolic pathway is well documented, but that of glucosamine (GlcN) is currently unknown. Importantly, GlcN is lethal to Streptomyces coelicolor nagB mutants, which lack glucosamine-6-phosphate deaminase activity. Here we report that spontaneous and directed mutations in the gene for the ROK-family protein RokL6 (SCO1447) relieve GlcN toxicity in nagB mutants of S. coelicolor. RNA sequencing, ChIP-Seq and over-expression studies revealed that RokL6 acts by directly repressing SCO1448, which encodes a sugar exporter; RokL6 thereby only binds to the rokL6-SCO1448 intergenic region in vivo, with consensus binding site C(T)TATCAGG - 7 nt - CCTGATAG(A). The exact transcriptional start sites for rokL6 and SCO1448 were determined using 5’RACE. RokL6 represses the transcription of both rokL6 and SCO1448 by binding to overlapping promoter sequences. Taken together, our data show that RokL6 and SCO1448 are novel GlcN-related genes, whereby RokL6 directly controls the transcription of SCO1448. The latter is a key protein in the defense of S. coelicolor against the toxicity of GlcN in a nagB-mutant background, most likely via the export of GlcN-derived toxic intermediates.
2023-06-19 | GSE234437 | GEO
Project description:Abstract: Chitin, an insoluble polymer of GlcNAc, is an abundant source of carbon, nitrogen, and energy for marine microorganisms. Microarray expression profiling and mutational studies of Vibrio cholerae growing on a natural chitin surface, or with the soluble chitin oligosaccharides (GlcNAc)(2-6), GlcNAc, or the glucosamine dimer (GlcN)2 identified three sets of differentially regulated genes. We show that (i) ChiS, a sensor histidine kinase, regulates expression of the (GlcNAc)(2-6) gene set, including a (GlcNAc)2 catabolic operon, two extracellular chitinases, a chitoporin, and a PilA-containing type IV pilus, designated ChiRP (chitin-regulated pilus) that confers a significant growth advantage to V. cholerae on a chitin surface; (ii) GlcNAc causes the coordinate expression of genes involved with chitin chemotaxis and adherence and with the transport and assimilation of GlcNAc; (iii) (GlcN)2 induces genes required for the transport and catabolism of nonacetylated chitin residues; and (iv) the constitutively expressed MSHA pilus facilitates adhesion to the chitin surface independent of surface chemistry. Collectively, these results provide a global portrait of a complex, multistage V. cholerae program for the efficient utilization of chitin. This SuperSeries is composed of the SubSeries listed below.
2006-03-08 | GSE4388 | GEO
Project description:The yeast-to-hypha transition is tightly associated with pathogenicity in many human pathogenic fungi, such as the model fungal pathogen Cryptococcus neoformans, which is responsible for approximately 180,000 deaths annually. In this pathogen, the yeast-to-hypha transition can be initiated by distinct stimuli: mating stimulation or glucosamine (GlcN), the monomer of cell wall chitosan. However, it remains poorly understood how the signal specificity for Cryptococcus morphological transition by disparate stimuli is ensured. Here, by integrating temporal expression signature analysis and phenome-based clustering evaluation, we demonstrate that GlcN specifically triggers a unique cellular response, which acts as a critical determinant underlying the activation of GlcN-induced filamentation (GIF). This cellular response is defined by an unusually hyperactive cell wall synthesis that is highly ATP-consuming. A novel cell surface protein Gis1 was identified as the indicator molecule for the GlcN-induced cell wall response. The Mpk1-directed cell wall pathway critically bridges global cell wall gene induction and intracellular ATP supply, ensuring the Gis1-dependent cell wall response and the stimulus specificity of GIF. We further reveal that the ability of Mpk1 to coordinate the cell wall response and GIF activation is conserved in different Cryptococcus pathogens. Phosphoproteomics-based profiling together with genetic and phenotypic analysis revealed that the Mpk1 kinase mediates the regulatory specificity of GIF through a coordinated downstream regulatory network centered on Skn7 and Crz1. Overall, our findings discover an unprecedented and conserved cell wall biosynthesis-dependent fungal differentiation commitment mechanism, which enables the signal specificity of pathogenicity-related dimorphism induced by GlcN in Cryptococcus pathogens.
2021-08-27 | GSE146435 | GEO
Project description:We investigated the metabolic regulation of mast cell (MC) functions to control them. MCs are sentinels of the immune system with functions involved not only in host defense but also, if not properly controlled, in MC disorders such as systemic mastocytosis (SM). We identified N-acetyl-D-glucosamine (GlcNAc or NAG) as both a circulating biomarker for SM severity and an oncometabolite that promotes uncontrolled degranulation and proliferation of MCs expressing the Kit kinase domain mutant allele, D816V, that is both an oncogene and characterizes patients with SM. Given the known role of GlcNAc-related protein glycosylation in modifying factors involved in epigenetic regulation of gene expression and the effects of GlcNAc on neoplastic MCs effector functions, we asked whether the increased susceptibility of KIT D816V MCs to GlcNAc was due to chromatin state changes.
2023-04-20 | GSE149106 | GEO