Редактирование: FN1

Fibronectin precursor (FN) (Cold-insoluble globulin) (CIG) [Contains: Anastellin; Ugl-Y1; Ugl-Y2; Ugl-Y3] [FN]

==Publications==

{{medline-entry
|title=Systems biology and network pharmacology of frailty reveal novel epigenetic targets and mechanisms.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31332237
|abstract=Frailty is an age-associated condition, characterized by an inappropriate response to stress that results in a higher frequency of adverse outcomes (e.g., mortality, institutionalization and disability). Some light has been shed over its genetic background, but this is still a matter of debate. In the present study, we used network biology to analyze the interactome of frailty-related genes at different levels to relate them with pathways, clinical deficits and drugs with potential therapeutic implications. Significant pathways involved in frailty: apoptosis, proteolysis, muscle proliferation, and inflammation; genes as [[FN1]], [[APP]], [[CREBBP]], [[EGFR]] playing a role as hubs and bottlenecks in the interactome network and epigenetic factors as HIST1H3 cluster and miR200 family were also involved. When connecting clinical deficits and genes, we identified five clusters that give insights into the biology of frailty: cancer, glucocorticoid receptor, [[TNF]]-α, myostatin, angiotensin converter enzyme, ApoE, interleukine-12 and -18. Finally, when performing network pharmacology analysis of the target nodes, some compounds were identified as potentially therapeutic (e.g., epigallocatechin gallate and antirheumatic agents); while some other substances appeared to be toxicants that may be involved in the development of this condition.
|mesh-terms=* Aging
* Apoptosis
* Cell Proliferation
* Epigenesis, Genetic
* Frailty
* Genes
* Humans
* Muscle, Smooth
* Pharmacology
* Proteolysis
* Signal Transduction
* Systems Biology

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6646318
}}
{{medline-entry
|title=Effects of Fibronectin 1 on Cell Proliferation, Senescence and Apoptosis of Human Glioma Cells Through the PI3K/AKT Signaling Pathway.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30048971
|abstract=The current study aimed to investigate the role by which fibronectin 1 ([[FN1]]) influences the cell cycle, senescence and apoptosis in human glioma cells through the PI3K/ AKT signaling pathway. Differentially expressed genes (DEGs) were identified based on gene expression data (GSE12657, GSE15824 and GSE45921 datasets) and probe annotation files from Gene Expression Omnibus. The DEGs were identified in connection with gene ontology (GO) enrichment analysis and with the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. The positive expression of the [[FN1]] protein was detected by immunohistochemistry. The glioma cell lines U251 and T98G were selected and assigned into blank, negative control (NC) and siRNA-[[FN1]] groups. A dual luciferase reporter gene assay was used to investigate the effects of [[FN1]] on transcriptional activity through the PI3K/AKT signaling pathway. An MTT assay was applied for the detection of cell proliferation, while flow cytometry was employed for cell cycle stage and cellular apoptosis detection. β-galactosidase staining was utilized to detect cellular senescence, a scratch test was applied to evaluate cell migration, and a transwell assay was used to analyze cell invasion. Western blotting and qRT-PCR methods were used to detect the protein and mRNA expression levels, respectively, of the [[FN1]] gene and the related genes in the PI3K/AKT pathway (PI3K, AKT and PTEN), the cell cycle (pRb, [[CDK4]] and Cyclin D1) and cell senescence (p16 and p21) among the collected tissues and cells. GSE12657 profiling revealed [[FN1]] to be the most upregulated gene in glioma. Regarding the GSE12657 and GSE15824 datasets, [[FN1]] gene expression was higher in glioma tissues than in normal tissues. GO enrichment analysis and KEGG pathway enrichment analysis indicated that [[FN1]] is involved in the synthesis of extracellular matrix (ECM) components and the PI3K/AKT signaling pathway. Verification was provided, indicating the role played by the [[FN1]] gene in the regulation of the PI3K/AKT signaling pathway, as silencing the [[FN1]] gene was found to inhibit cell proliferation, promote cell apoptosis and senescence, and reduce migration and invasion through the down-regulation of [[FN1]] gene expression and disruption of the PI3K-AKT signaling pathway. The findings of this study provide evidence highlighting the prominent role played by [[FN1]] in stimulating glioma growth, invasion, and survival through the activation of the PI3K/AKT signaling pathway.
|mesh-terms=* Adult
* Aged
* Apoptosis
* Brain Neoplasms
* Cell Line, Tumor
* Cell Proliferation
* Cellular Senescence
* Female
* Fibronectins
* Gene Expression Regulation, Neoplastic
* Glioma
* Humans
* Male
* Middle Aged
* Neoplasm Invasiveness
* Phosphatidylinositol 3-Kinases
* Proto-Oncogene Proteins c-akt
* Signal Transduction
|keywords=* Apoptosis
* Cell cycle
* Fibronectin 1
* Gene expression data
* Glioma
* PI3K/AKT signaling pathway
* Senescence
|full-text-url=https://sci-hub.do/10.1159/000492096
}}
{{medline-entry
|title=Enhanced tissue regeneration potential of juvenile articular cartilage.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24043472
|abstract=Articular cartilage undergoes substantial age-related changes in molecular composition, matrix structure, and mechanical properties. These age-related differences between juvenile and adult cartilage manifest themselves as markedly distinct potentials for tissue repair and regeneration. To compare the biological properties and tissue regeneration capabilities of juvenile and adult bovine articular cartilage. Controlled laboratory study. Articular cartilage harvested from juvenile (age, 4 months) and adult (age, 6-8 years) bovine femoral condyles was cultured for 4 weeks to monitor chondrocyte migration, glycosaminoglycan content conservation, and new tissue formation. The cartilage cell density and proliferative activity were also compared. Additionally, the effects of age-related changes on cartilage gene expression were analyzed using the Affymetrix GeneChip array. Compared with adult cartilage, juvenile bovine cartilage demonstrated a significantly greater cell density, higher cell proliferation rate, increased cell outgrowth, elevated glycosaminoglycan content, and enhanced matrix metallopeptidase 2 activity. During 4 weeks in culture, only juvenile cartilage was able to generate new cartilaginous tissues, which exhibited pronounced labeling for proteoglycan and type II collagen but not type I collagen. With over 19,000 genes analyzed, distinctive gene expression profiles were identified. The genes mostly involved in cartilage growth and expansion, such as [[COL2A1]], [[COL9A1]], [[MMP2]], [[MMP14]], and [[TGFB3]], were upregulated in juvenile cartilage, whereas the genes primarily responsible for structural integrity, such as [[COMP]], [[FN1]], [[TIMP2]], [[TIMP3]], and [[BMP2]], were upregulated in adult cartilage. As the first comprehensive comparison between juvenile and adult bovine articular cartilage at the tissue, cellular, and molecular levels, the results strongly suggest that juvenile cartilage possesses superior chondrogenic activity and enhanced regenerative potential over its adult counterpart. Additionally, the differential gene expression profiles of juvenile and adult cartilage suggest possible mechanisms underlying cartilage age-related changes in their regeneration capabilities, structural components, and biological properties. The results of this comparative study between juvenile and adult bovine articular cartilage suggest an enhanced regenerative potential of juvenile cartilage tissue in the restoration of damaged articular cartilage.
|mesh-terms=* Aging
* Animals
* Cartilage, Articular
* Cattle
* Cell Count
* Cell Proliferation
* Chondrocytes
* Gene Expression Profiling
* Glycosaminoglycans
* Matrix Metalloproteinase 2
* Oligonucleotide Array Sequence Analysis
* Regeneration
|keywords=* adult
* aging
* articular cartilage
* biology of cartilage
* bovine
* cartilage regeneration
* cartilage repair
* chondrocyte
* gene expression
* juvenile
* knee
* migration
|full-text-url=https://sci-hub.do/10.1177/0363546513502945
}}
{{medline-entry
|title=Polyploidy impairs human aortic endothelial cell function and is prevented by nicotinamide phosphoribosyltransferase.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/19846757
|abstract=Polyploid endothelial cells are found in aged and atherosclerotic arteries. However, whether increased chromosome content has an impact on endothelial cell function is unknown. We show here that human aortic endothelial cells become tetraploid as they approach replicative senescence. Furthermore, accumulation of tetraploid endothelial cells was accelerated during growth in high glucose. Interestingly, induction of polyploidy was completely prevented by modest overexpression of the NAD  regenerating enzyme, nicotinamide phosphoribosyltransferase (Nampt). To determine the impact of polyploidy on endothelial cell function, independent of replicative senescence, we induced tetraploidy using the spindle poison, nocodazole. Global gene expression analyses of tetraploid endothelial cells revealed a dysfunctional phenotype characterized by a cell cycle arrest profile (decreased CCNE2/A2, [[RBL1]], BUB1B; increased CDKN1A) and increased expression of genes involved in inflammation (IL32, TNFRSF21/10C, PTGS1) and extracellular matrix remodeling (COL5A1, [[FN1]], MMP10/14). The protection from polyploidy conferred by Nampt was not associated with enhanced poly(ADP-ribose) polymerase-1 or sirtuin (SIRT) 2 activity, but with increased [[SIRT1]] activity, which reduced cellular reactive oxygen species and the associated oxidative stress stimulus for the induction of polyploidy. We conclude that human aortic endothelial cells are prone to chromosome duplication that, in and of itself, can induce characteristics of endothelial dysfunction. Moreover, the emergence of polyploid endothelial cells during replicative aging and glucose overload can be prevented by optimizing the Nampt-[[SIRT1]] axis.
|mesh-terms=* Aging
* Aorta
* Atherosclerosis
* Cell Cycle
* Cell Division
* Cytokines
* Endothelium, Vascular
* Extracellular Matrix
* Gene Expression Regulation
* Genes, Reporter
* Glucose
* Humans
* Inflammation
* Nicotinamide Phosphoribosyltransferase
* Nocodazole
* Polyploidy

|full-text-url=https://sci-hub.do/10.1152/ajpcell.00357.2009
}}
{{medline-entry
|title=The signaling hubs at the crossroad of longevity and age-related disease networks.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/18793745
|abstract=The established human age-related disease proteins (ARDPs) and longevity-associated proteins (LAPs) together with their first-order interacting partners form scale-free networks which significantly overlap. About half of the common proteins are involved in signal transduction. These proteins are strongly interconnected and in turn form a common signaling network which comprises over 40% of all hubs (proteins with multiple interactions) in the human interactome. Along with the insulin pathway, the common signaling network is remarkably enriched with the focal adhesion and adherens junction proteins whose relation to the control of lifespan is yet to be fully addressed. The examples of such candidate proteins include several hubs, focal adhesion kinase [[PTK2]] and the extracellular proteins fibronectin [[FN1]], paxillin [[PXN]], and vinculin [[VCL]]. The results of the network-based analysis highlight the potential importance of these pathways, especially hubs, in linking the human longevity and age-related diseases.
|mesh-terms=* Adherens Junctions
* Aging
* Alzheimer Disease
* Animals
* Atherosclerosis
* Diabetes Mellitus, Type 2
* Fibronectins
* Focal Adhesion Kinase 1
* Focal Adhesions
* Humans
* Longevity
* Paxillin
* Protein Interaction Domains and Motifs
* Signal Transduction
* Vinculin

|full-text-url=https://sci-hub.do/10.1016/j.biocel.2008.08.026
}}
{{medline-entry
|title=Age-specific hormonal decline is accompanied by transcriptional changes in human sebocytes in vitro.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/16805856
|abstract=The importance of hormones in endogenous aging has been displayed by recent studies performed on animal models and humans. To decipher the molecular mechanisms involved in aging we maintained human sebocytes at defined hormone-substituted conditions that corresponded to average serum levels of females from 20 (f20) to 60 (f60) years of age. The corresponding hormone receptor expression was demonstrated by reverse transcription-polymerase chain reaction (RT-PCR), Western blotting and immunocytochemistry. Cells at f60 produced significantly lower lipids than at f20. Increased mRNA and protein levels of c-Myc and increased protein levels of [[FN1]], which have been associated with aging, were detected in SZ95 sebocytes at f60 compared to those detected at f20 after 5 days of treatment. Expression profiling employing a cDNA microarray composed of 15 529 cDNAs identified 899 genes with altered expression levels at f20 vs. f60. Confirmation of gene regulation was performed by real-time RT-PCR. The functional annotation of these genes according to the Gene Ontology identified pathways related to mitochondrial function, oxidative stress, ubiquitin-mediated proteolysis, cell cycle, immune responses, steroid biosynthesis and phospholipid degradation - all hallmarks of aging. Twenty-five genes in common with those identified in aging kidneys and several genes involved in neurodegenerative diseases were also detected. This is the first report describing the transcriptome of human sebocytes and its modification by a cocktail of hormones administered in age-specific levels and provides an in vitro model system, which approximates some of the hormone-dependent changes in gene transcription that occur during aging in humans.
|mesh-terms=* Aging
* Cell Line
* Cell Proliferation
* Chromosomes, Human
* Fibronectins
* Gene Expression Profiling
* Gene Expression Regulation
* Hormones
* Humans
* Oligonucleotide Array Sequence Analysis
* Proto-Oncogene Proteins c-myc
* Sebaceous Glands
* Signal Transduction
* Transcription, Genetic

|full-text-url=https://sci-hub.do/10.1111/j.1474-9726.2006.00223.x
}}
{{medline-entry
|title=Auditory brain map, effects of age.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/3227262
|abstract=Brain maps of late auditory evoked cortical potentials were obtained with the Brain Atlas III system in school-aged children and adults. All subjects were judged as neurologically normal, right-handed, and having normal hearing. The stimulus was a 100 ms burst of 500 Hz pure tone at 75 dB HL presented separately to the left and right ear. The results showed a frontoparietal maximum of negative activity corresponding to N1 and designated as the focus of N1 ([[FN1]]). [[FN1]] had latencies of 108 ms (left stimulation (stim] and 113 ms (right stim) and amplitudes of -6.0 microV (left stim) and -4.8 microV (right stim) in children and a latency of 90 ms and an amplitude of -6.5 microV in adults. Among the children, more had ipsilateral than contralateral [[FN1]], usually on the right side. The distance between the centers of gravity of [[FN1]]s obtained on stimulation of the two ears was significantly smaller in the maps of children than adults (p less than 0.01). The present findings indicated that the topography of the electrical activity changes during adolescence.
|mesh-terms=* Adult
* Aging
* Brain Mapping
* Child
* Electroencephalography
* Evoked Potentials, Auditory
* Female
* Hearing
* Humans
* Male
* Middle Aged
* Reference Values


}}