Role of transglutaminase 2 in promoting biglycan synthesis in idiopathic gingival fibromatosis
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ABSTRACT:
PROVIDER: PRJNA1162834 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30724565_1.fastq.gz | Fastqsanger.gz | |||
| SRR30724565_2.fastq.gz | Fastqsanger.gz | |||
| SRR30724566_1.fastq.gz | Fastqsanger.gz | |||
| SRR30724566_2.fastq.gz | Fastqsanger.gz | |||
| SRR30724567_1.fastq.gz | Fastqsanger.gz |
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Project description:The mechanism of idiopathic gingival fibromatosis is still unclear. To provide new insights into the molecular and cellular differences between idiopathic gingival fibromatosis and periodontitis, we first identified the gene TGM2, which is differentially expressed between the two. We found that the expression of TGM2 is predominantly lower in idiopathic gingival fibromatosis than in periodontitis, and that the activity of SP1 due to the decreased expression of TGM2 promotes the generation of extracellular matrix-related genes in idiopathic gingival fibromatosis. We have identified biglycan, an extracellular matrix that is specifically upregulated in idiopathic gingival fibromatosis, and highlight the effects of SP1 and TGM2 on biglycan expression.
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Project description:Gingival fibromatosis (GF) is a rare oral condition characterized by proliferative fibrous overgrowth of both the attached and marginal gingiva, and the interdental papilla. But there were no papers about gene expression of gingival fibromatosis. The aim of this study was to identify the differential expression of genes in GF using cDNA microarray analysis.
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Project description:The enamel renal syndrome (ERS) is a rare disorder featured by amelogenesis imperfecta, gingival fibromatosis and nephrocalcinosis. Gingival fibromatosis is a hallmark of the disease; it is characterized by the accumulation of a collagen-rich, dense connective tissue and of mineral deposits throughout the gingiva. ERS is caused by biallelic mutations in the FAM20A gene encoding a pseudokinase, likely acting as an allosteric activator of FAM20C, the Golgi casein kinase. How mutations in FAM20A may modify the gingival connective tissue homeostasis and cause fibromatosis is currently unknown. Conditioned media of gingival fibroblasts (GF) obtained from four unrelated ERS patients carrying distinct mutations and three control subjects were used. Secretomic analysis identified 109 dysregulated proteins whose abundance had increased (69 proteins) or decreased (40 proteins) at least 1.5-fold compared to control GF. Gene Ontology (GO) analysis revealed biological processes significantly over-represented or under-represented in the ERS GF. Proteins over-represented were mainly involved in extracellular matrix organization, collagen fibril assembly, and biomineralization whereas those under-represented were extracellular matrix-associated proteins. Accordingly, GO disease analysis indicated un significant enrichment of tumoral angiogenesis and fibrosis.
2022-02-17 | PXD028003 | Pride
Project description:To identify dysregulated genes in HGF (Hereditary Gingival Fibromatosis) patients, expression profiling was performed using Affymetrix Human Genome U133 plus 2.0 arrays. Total RNA was extracted from gingival tissue specimens excised from two non-syndromic HGF patients, siblings in one family, and three normal controls. Quantity and integrity of the total RNA was measured and assessed by Nanodrop spectrophotometer (Thermo Fisher Scientific) and agarose gel electrophoresis. In brief, cDNA preparation, cRNA labeling, hybridization to Affymetrix Human Genome U133 plus 2.0 arrays, and chip scanning were performed in accordance with the manufacturer’s protocol (Affymetrix). *.CEL data from the raw chip scans were imported into the Partek GS 6.5 and normalized by RMA normalization algorithms. Comparisons between the HGF and control group were performed with one-way ANOVA (p≤0.05).
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Project description:This study examines the expression profile of cells from human aggressive fibromatosis tumors.
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Project description:This study examines the expression profile of cells from human aggressive fibromatosis tumors. Cells from human aggressive fibromatosis tumors were manually minced, and visible clumps were removed. Enzymatic digestion using 10 mg/mL of collagenase IV, 2.4 units/mL Dispase, 0.05% trypsin, was used for 45 min at 37°C. Cells were then centrifuged at 1400 rpm for 5 min and washed thrice in PBS. RNA was extracted using RNA was extracted using Trisol as per the manufacturer's instructions, and used for gene profiling studies.
2014-12-22 | E-GEOD-23356 | biostudies-arrayexpress
Project description:There were no studies about gene expression of normal gingiva before. We performed this study to compare with gene expression of gingival fibromatosis
2017-02-12 | GSE58480 | GEO
Project description:All experiment was done according to the Affymetrix manufacturerâs protocol. The resulting HGF gingiva expression profile(Hereditary gingival fibromatosis patient Gingiva replicate1 and replicate 2)was compared to normal gingiva control(Normal Gingiva replicate1 and replicate2). The data were collected and analyzed by GCOS 1.2 and GeneSpring 7.2 1-way T test. Experiment Overall Design: Hereditary gingival fibromatosis patient Gingiva (experimental) and Normal Gingiva (control) were used. N1 and P1 are gingiva tissue from female individuals while N2 and P2 are from male ones.
2008-06-12 | E-GEOD-4250 | biostudies-arrayexpress
Project description:Gingival fibromatosis is a rare and heterogeneous group of disorders that develop as slowly progressive, local or diffuse enlargements within marginal and attached gingiva or interdental papilla. In severe cases, the excess tissue may cover the crowns of the teeth, thus causing functional, esthetic, and periodontal problems, such as bone loss and bleeding, due to the presence of pseudopockets and plaque accumulation. It affects both genders equally. Hereditary, drug-induced, and idiopathic gingival overgrowth have been reported. Hereditary gingival fibromatosis can occur as an isolated condition or as part of a genetic syndrome. The pathologic manifestation of gingival fibromatosis comprises excessive accumulation of extracellular matrix proteins, of which collagen type I is the most prominent example. Mutation in the Son-of-Sevenless-1 gene has been suggested as one possible etiological cause of isolated (non-syndromic) hereditary gingival fibromatosis, but mutations in other genes are also likely to be involved, given the heterogeneity of this condition. The most attractive concept of mechanism for drug-induced gingival overgrowth is epithelial-to-mesenchymal transition, a process in which interactions between gingival cells and the extracellular matrix are weakened as epithelial cells transdifferentiate into fibrogenic fibroblast-like cells. The diagnosis is mainly made on the basis of the patient's history and clinical features, and on histopathological evaluation of affected gingiva. Early diagnosis is important, mostly to exclude oral malignancy. Differential diagnosis comprises all pathologies in the mouth with excessive gingival overgrowth. Hereditary gingival fibromatosis may present as an autosomal-dominant or less commonly autosomal-recessive mode of inheritance. If a systemic disease or syndrome is suspected, the patient is directed to a geneticist for additional clinical examination and specialized diagnostic tests. Treatments vary according to the type of overgrowth and the extent of disease progression, thus, scaling of teeth is sufficient in mild cases, while in severe cases surgical intervention is required. Prognosis is precarious and the risk of recurrence exists.
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Project description:We examined gene expression signatures in healthy and diseased gingival tissues in 90 patients. Analysis of the gingival tissue transcriptome in states of periodontal health and disease may reveal novel insights of the pathobiology of periodontitis. Keywords: gingival tissue disease state analysis
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