Reduction of ETV1 is Identified as a Prominent Feature of Age-Related Cataract.

PURPOSE: To identify the inactive genes in cataract lenses and explore their function in lens epithelial cells (LECs). METHODS: Lens epithelium samples obtained from both age-related cataract (ARC) patients and normal donors were subjected to two forms of histone H3 immunoprecipitation: H3K9ac and H3K27me3 chromatin immunoprecipitation (ChIP), followed by ChIP-seq. The intersection set of "active genes in normal controls" and "repressed genes in cataract lenses" was identified. To validate the role of a specific gene, ETV1, within this set, quantitative polymerase chain reaction (qPCR), western blot, and immunofluorescence were performed using clinical lens epithelium samples. Small interference RNA (siRNA) was utilized to reduce the mRNA level of ETV1 in cultured LECs. Following this, transwell assay and western blot was performed to examine the migration ability of the cells. Furthermore, RNA-seq analysis was conducted on both cell samples with ETV1 knockdown and control cells. Additionally, the expression level of ETV1 in LECs was examined using qPCR under H2O2 treatment. RESULTS: Six genes were identified in the intersection set of "active genes in normal controls" and "repressed genes in ARC lenses". Among these genes, ETV1 showed the most significant fold-change decrease in the cataract samples compared to the control samples. After ETV1 knockdown by siRNA in cultured LECs, reduced cell migration was observed, along with a decrease in the expression of ß-Catenin and Vimentin, two specific genes associated with cell migration. In addition, under the oxidative stress induced by H2O2 treatment, the expression level of ETV1 in LECs significantly decreased. CONCLUSIONS: Based on the findings of this study, it can be concluded that ETV1 is significantly reduced in human ARC lenses. The repression of ETV1 in ARC lenses appears to contribute to the disrupted differentiation of lens epithelium, which is likely caused by the inhibition of both cell differentiation and migration processes.

Variations in protein expression associated with oral cancer.

BACKGROUND: Differential protein expression of the oral microbiome is related to human diseases, including cancer. OBJECTIVE: In order to reveal the potential relationship between oral bacterial protein expression in oral squamous cell carcinoma (OSCC), we designed this study. METHODS: We obtained samples of the same patient from cancer lesion and anatomically matched normal site. Then, we used the label free quantitative technique based on liquid chromatography tandem mass spectrometry (LC-MS/MS) to analyze the bacteria in the samples of oral squamous cell carcinoma at the protein level, so as to detect the functional proteins. RESULTS: Protein diversity in the cancer samples was significantly greater than in the normal samples. We identified a substantially higher number of the taxa than those detected in previous studies, demonstrating the presence of a remarkable number of proteins in the groups. In particular, proteins involved in energy production and conversion, proton transport, hydrogen transport and hydrogen ion transmembrane transport, ATP-binding cassette (ABC) transporter, PTS system, and L-serine dehydratase were enriched significantly in the experimental group. Moreover, some proteins associated with Actinomyces and Fusobacterium were highly associated with OSCC and provided a good diagnostic outcome. CONCLUSION: The present study revealed considerable changes in the expression of bacterial proteins in OSCC and enrich our understanding in this point.

DNA methylation profile of lip tissue from congenital nonsyndromic cleft lip and palate patients by whole-genome bisulfite sequencing.

Congenital nonsyndromic cleft lip and palate (NSCLP) is one of the most common malformations worldwide. DNA methylation has been implicated in many diseases. However, its involvement in lip tissue from NSCLP is not well understood. This study aimed to investigate the role of dysregulated DNA methylation in NSCLP. DNA methylation profile was determined in eight injured and five self-normal lip tissue samples from children with NSCLP by whole-genome bisulfite sequencing. A total of 2,711 differentially methylated regions (DMRs), corresponding to 1,231 genes were identified. Given the important role of promoter methylation in regulating gene expression, the promoter DMR-related genes were considered. Bioinformatics analysis demonstrated that some of them showed potential associations with NSCLP. Therefore, the well-known NSCLP susceptibility gene, GLI family zinc finger 2 (GLI2) with an unknown role in its DNA methylation in NSCLP, was selected for further analysis. The promoter hypomethylation and higher mRNA expression level of GLI2 were observed in injured lip tissues by verification in additional samples. Moreover, dual luciferase reporter assay indicated that promoter hypermethylation of GLI2 inhibited its transcription. Overall, this study suggested that abnormal DNA methylation in lip tissue may be correlated with the pathogenesis of congenital NSCLP.

[Research on histologic changes of periodontal tissue, testification of TNF-alpha and their relationship in diabetics rats].

OBJECTIVE: The histologic and TNF-alpha changes of the experimental periodontitis were studied in diabetic rat model in different periods. The mechanism of the occurring and developing of periodontitis was probed on the aspect of cytology. METHODS: The diabetic rat models were established by injecting streptozotocin into its abdomen. The local stimulation was caused by tiring silk thread to teeth. The histologic changes of periodontium were observed at 6,9,and 12 weeks. The level of TNF-alpha was testified using immunohistochemistry method at 12 weeks. RESULTS: Periodontitis occurred in diabetic rats earlier than in non-diabetic ones. The destructions were more severe and more widely in diabetic rats than in non-diabetic ones. The level of TNF-alpha was higher in the experimental periodontium of diabetic rats than those non-diabetics. CONCLUSIONS: Diabetes mellitus has an accelerating effect on occurring and developing of periodontitis. When with diabetes, more cytokines were released, and cause the unbalance of ruin and repair and result in the enhancing of periodontitis.