Project description:The expression profile of miRNAs in soft palate muscle of patients with OSAHS (obstructive sleep apnea/hypopnea syndrome) and chronic tonsillitis was examined using miRNA microarray analysis. Combining with the following real time PCR and bioinformatics analysis, the physiological importance of the miRNA-autophagy interconnection is far more likely to be elucidated.
Project description:We report the application of single cell transcriptome, bulk transcriptome, and chromatin accessibility analysis for investigating the role of Runx2 in regulating soft palate muscle development. By isolating single cells from soft palate tissue of wild type embryos at E13.5, E14.5 and E15.5, we describe the heterogeneity of soft palate mesenchyme during development by analyzing single cell transcriptome. Combined analysis of bulk and single cell transcriptome of soft palate from wild type and Runx2 mutant suggests Runx2 activate expression of perimysial markers. Finally, we show that Runx2 activates expression of perimysial markers probably by repressing Twist1 through chromatin accessibility analysis. This study provides the first single cell level heterogeneity analysis of developing soft palate and shows the important role of Runx2 in regulating soft palate muscle development.
Project description:In order to investigate the gene expression patterns and molecular regulatory mechanisms of obstructive sleep apnea hypopnea syndrome (OSAHS), the global transcriptome expression profiles of OSAHS patients and healthy people were analyzed using transcriptome sequencing technology. Differential expression of circular RNA, microRNA, long noncoding RNA, and messenger RNA was investigated between the two groups.
Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in epithelial cells as it pertains to the orientation of muscle fibers in the soft palate during embryogenesis. Here, we first conducted gene expression profiling of the anterior and posterior portions of the palate from wild-type mice. In addition, we also conducted gene expression profiling of the posterior palate in mutant mice with an epithelium-specific conditional inactivation of the Tgfbr2 gene. The latter mice provide a model of submucosal cleft palate, which is a congenital birth defect commonly observed in many syndromic conditions.
