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.
Project description:OSAHS is a complex,synthetical disease that can lead to multiple system and multiple organ damage as the disease progresses.Metabolic syndrome is the most common complication, but the symptoms at different stages of the disease are different.It is known that miRNAs can be stably in the serum and changes during the development of the disease.Therefore, we speculate that serum miRNAs could biomarkers for OSAHS diagnosis and progression judgment. We used microarrays to detail the miRNA expression of simple OSAHS patients, OSAHS patients with hypertension and healthy controls, and screened out the miRNAs that were differentially expressed between the two groups.
Project description:To identify distinctive miRNA signatures in OSAHS with Mets patients from healthy subjects, that could serve as diagnostic biomarkers or describe differential molecular mechanisms with potential therapeutic implications. 5 OSAHS with metabolic syndrome (MetS) patients and 4 Tibetan healthy subjects were selected as the control group from January 2018 to January 2021, who signed an informed, written consent form. All OSAHS Patients diagnosed by Polysomnography (PSG). Patients suffering from other respiratory diseases, or combined with allergic and autoimmune diseases, tumors and other serious systemic serious primary diseases were excluded from this study. Plasma was isolated and frozen at -80 ◦C.
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. To investigate the adverse effects of dysfunctional TGF-Beta signaling on tissue-tissue interaction between the palatal epithelium and myofibers during palatogenesis, we analyzed mice with an epithelial cell-specific conditional inactivation of Tgfbr2 (Tgfbr2fl/fl;K14-Cre). We performed microarray analyses of anterior palatal tissue and posterior palatal tissue of E15.5 Tgfbr2fl/fl control mice (n=5, each region), and posterior palatal tissue of Tgfbr2fl/fl;K14-Cre mutant mice, collected at embryonic day 15.5 (n=5). Control samples and mutant samples are from separate litters.
Project description:Transcriptome and chromatin accessiblity analysis of mice soft palate to unreveal the role of Runx2 in regulating palate muscle development.
Project description:Craniofacial development depends on cell-cell interactions, coordinated cellular movement and differentiation under the control of regulatory gene networks, which include the distal-less (Dlx) gene family. However, the functional significance of Dlx5 in patterning the oropharyngeal region has remained unknown. Here we show that loss of Dlx5 leads to a shortened soft palate and an absence of the levator veli palatini, palatopharyngeus, and palatoglossus muscles that are derived from the 4th pharyngeal arch (PA), but the tensor veli palatini, derived from the 1st PA, is unaffected. Dlx5-positive cranial neural crest (CNC) cells are in direct contact with myoblasts derived from the pharyngeal mesoderm, and Dlx5 disruption leads to altered proliferation and apoptosis of CNC and muscle progenitor cells. Moreover, the FGF10 pathway is downregulated in Dlx5-/- mice, and activation of FGF10 signaling rescues CNC cell proliferation and myogenic differentiation in these mutant mice. Collectively, our results indicate that Dlx5 plays critical roles in patterning of the oropharyngeal region and development of muscles derived from the 4th PA mesoderm in the soft palate, likely via interactions between CNC-derived and myogenic progenitor cells.
