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Mouse myoblasts grown on Fibronectin or Collagen I for 72 hours

ABSTRACT: The goal of this study was to investigate the transcriptional regulation in cells grown on Fibronectin when compared to Collagen I 3 samples per condition

ORGANISM(S): Mus musculus

SUBMITTER: Jerome Feige

PROVIDER: E-GEOD-81225 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Loss of fibronectin from the aged stem cell niche affects the regenerative capacity of skeletal muscle in mice.

Lukjanenko Laura L Jung M Juliane MJ Hegde Nagabhooshan N Perruisseau-Carrier Claire C Migliavacca Eugenia E Rozo Michelle M Karaz Sonia S Jacot Guillaume G Schmidt Manuel M Li Liangji L Metairon Sylviane S Raymond Frederic F Lee Umji U Sizzano Federico F Wilson David H DH Dumont Nicolas A NA Palini Alessio A Fässler Reinhard R Steiner Pascal P Descombes Patrick P Rudnicki Michael A MA Fan Chen-Ming CM von Maltzahn Julia J Feige Jerome N JN Bentzinger C Florian CF

Nature medicine 20160704 8

Age-related changes in the niche have long been postulated to impair the function of somatic stem cells. Here we demonstrate that the aged stem cell niche in skeletal muscle contains substantially reduced levels of fibronectin (FN), leading to detrimental consequences for the function and maintenance of muscle stem cells (MuSCs). Deletion of the gene encoding FN from young regenerating muscles replicates the aging phenotype and leads to a loss of MuSC numbers. By using an extracellular matrix (E ...[more]

PMID: 27376579

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Mouse myoblasts grown on Fibronectin or Collagen I for 72 hours

Project description:The goal of this study was to investigate the transcriptional regulation in cells grown on Fibronectin when compared to Collagen I

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2008-04-05 | E-GEOD-10227 | biostudies-arrayexpress

Site-specific N- and O-glycosylation Analysis of Human Plasma Fibronectin

Project description:Human plasma fibronectin is an adhesive protein that plays a crucial role in wound healing. Many studies had indicated that glycans may mediate the expression and functions of fibronectin, yet a comprehensive understanding of its glycosylation is still missing. Here, we performed a comprehensive N- and O-glycosylation mapping of human plasma fibronectin, and quantified the occurrence of each glycoform in a site-specific manner. Intact N-glycopeptides were enriched by zwitterionic hydrophilic interaction chromatography, and N-glycosites sites were localized by the 18O-labeling method. O-glycopeptide enrichment and O-glycosite identification were achieved by an enzyme-assisted site-specific extraction method. An RP–LC–MS/MS system functionalized with Collision-Induced Dissociation and stepped normalized collision energy (sNCE)-HCD tandem mass was applied to analyze the glycoforms of fibronectin. A total of 6 N-glycosites and 53 O-glycosites were identified, which were occupied by 3842 N-glycoforms and 16 O-glycoforms, respectively. Furthermore, 81.4% of N-glycans were either fucosylated, sialylated, or with both modifications77.31% of N-glycans were sialylated, while O-glycosylation was dominated by the sialyl-T antigen. These site-specific glycosylation patterns on human fibronectin can facilitate functional analyses of fibronectin and therapeutics development.

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Fibronectin Induced Cardiac Myocyte Hypertrophy

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Transcription profiling of rat neonatal ventricular myocytes plated in fibronectin reveals fibronectin induced cardiac myocyte hypertrophy

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Protein expression in primary murine dermal fibroblasts grown on fibronectin vs. plastic

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DECREASED FIBRONECTIN PRODUCTION SIGNIFICANTLY CONTRIBUTES TO DYSREGULATED REPAIR OF ASTHMATIC EPITHELIUM

Project description:Rationale: Damage to airway epithelium is followed by deposition of extracellular matrix (ECM) and migration of adjacent epithelial cells. We have shown that epithelial cells from asthmatic children fail to heal a wound in vitro. Objectives: To determine whether dysregulated ECM production by the epithelium plays a role in aberrant repair in asthma. Methods: Airway epithelial cells (AEC) from children with asthma (n=36), healthy atopic (n=23) and healthy non-atopic controls (n=53) were investigated by microarray, gene expression and silencing, transcript regulation analysis and ability to close mechanical wounds. Results: Wound repair of AEC from healthy and atopic children were not significantly different and were both faster than AEC from asthmatics. Microarray analysis revealed differential expression of multiple gene sets associated with repair and remodeling in asthmatic AEC. Fibronectin (FN) was the only ECM component whose expression was significantly lower in asthmatic AEC. Expression differences were verified by qPCR and ELISA, and reduced FN expression persisted in asthmatic cells over passage. Silencing of FN expression in non-asthmatic AEC inhibited wound repair, while addition of FN to asthmatic AEC restored reparative capacity. Asthmatic AEC failed to synthesize FN in response to wounding or cytokine/growth factor stimulation. Exposure to 5â, 2âdeoxyazacytidine had no effect on FN expression and subsequent analysis of the FN promoter did not show evidence of DNA methylation. Conclusions: These data show that the reduced capacity of asthmatic epithelial cells to secrete FN is an important contributor to the dysregulated AEC repair observed in these cells. 16 arrays, 2 experimental groups, asthma atopic, AA, and healthy non-atopic, HN.

2010-04-12 | E-GEOD-18965 | biostudies-arrayexpress

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