Determination of expression level of gingiva expressed genes
Ontology highlight
ABSTRACT: All experiment was done according to the Affymetrix manufacturer’s 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. Keywords: tissue specific expression profile
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.
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
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.
Project description:Purpose: The goal of this study was to characterize the gingival oral barrier immunity of mouse periodontitis gingiva. Method: A silk thread (ligature) was tied wround the mouse maxillary molar. Mouse palatal gingiva was harvested at 1 days after the ligature placement. Gingival cells were harvested and subjected to 10X Genomix scRNA-seq. Cell Ranger processed data were analysed.
Project description:Purpose: The goal of this study was to characterize the gingival oral barrier immunity of mouse early periodontitis gingiva. Method: A silk thread (ligature) was tied wround the mouse maxillary molar. Mouse palatal gingiva was harvested at 1 days after the ligature placement. Gingival cells were harvested and subjected to 10X Genomix scRNA-seq. Cell Ranger processed data were analysed.
Project description:The periodontium undergoes age-related cellular and clinical changes, but the involved genes are not yet known. Here, we investigated age-related genetic changes in gingiva at the transcriptomic level. Genes that were differentially expressed between young and old human gingiva were identified by RNA sequencing and verified by real-time PCR. A total of 1939 mRNA transcripts showed significantly differential expression between young and old gingival tissues. Matrix metalloprotease (MMP) regulation was the top pathway involved in gingival aging. MMP3, MMP9, MMP12, and MMP13 were upregulated in old gingival tissues, concomitantly with interleukin-1 beta (IL1B) expression. In vitro experiments using human gingival fibroblasts (hGFs) showed that MMP12 was upregulated in old hGFs compared to young hGFs. Moreover, the MMP3, MMP9 and IL1B levels were more highly stimulated by infection with the oral bacterium, Fusobacterium nucleatum, in old hGFs compared to young hGFs. Collectively, these findings suggest that, in gingiva, the upregulation of MMP12 may be a molecular hallmark of natural aging, while the upregulations of MMP3, MMM9, and IL1B may indicate externally (e.g., infection)-induced aging. These findings contribute to our understanding of the molecular targets involved in gingival aging.
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).
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.
Project description:Purpose: The goal of this study was to characterize the gingival oral barrier immunity of TLR9 ligand (CpG oligonucleotide) and TLR2/4 ligand (LPS)-treated mouse maxilla. Method: TLR9 ligand or TLR2/4 ligand was topically applied to the mouse palatal gingiva. Mouse palatal gingiva was harvested at 4 days after topical application. Gingival cells were harvested and subjected to 10X Genomix scRNA-seq. Cell Ranger processed data were analysed.