Project description:To investigate the functions of ncRNAs in temporomandibular joint osteoarthritis, we established temporomandibular joint osteoarthritis model induced by unilateral anterior crossbite. We then performed gene expression profiling analysis using data obtained from RNA-seq of condylar cartilage at 8 weeks of modeling.
Project description:To investigate the functions of ncRNAs in temporomandibular joint osteoarthritis, we established temporomandibular joint osteoarthritis model induced by unilateral anterior crossbite. We then performed gene expression profiling analysis using data obtained from RNA-seq of condylar cartilage at 8 weeks of modeling.
Project description:To investigate the mechanisms underlying cloned placenta hyperplasia, we employed single-nuclei RNA and ATAC-seq multi-omics at the critical window of placental overgrowth. Our work offers the first comprehensive and novel single-nuclei–level dissection of developmental barriers in SCNT placentas, demonstrating that genomic instability constitutes the principal determinant of SCNT placental dysfunction, and outlines a feasible approach to improve reproductive cloning outcomes.
Project description:To investigate the mechanisms underlying cloned placenta hyperplasia, we employed single-cell RNA and ATAC-seq multi-omics at the critical window of placental overgrowth. Our work offers the first comprehensive and novel single-cell–level dissection of developmental barriers in SCNT placentas, demonstrating that genomic instability constitutes the principal determinant of SCNT placental dysfunction, and outlines a feasible approach to improve reproductive cloning outcomes.
Project description:Epithelial tumors can progress from a benign tissue overgrowth (hyperplasia) to a malignant neoplastic tumor, which is characterized by an increase in motility and invasiveness. The Cohen laboratory has developed an epithelial tumor model in which overexpression of the epidermal growth factor receptor gene (EGFR) leads to benign tissue hyperplasia. When combined with other cooperating factors, EGFR overexpression can lead to neoplasia and malignant metastasis. Microarray analysis were performed in normal epithelia, hyperplastic, and neoplastic tumors collected from Drosophila wing imaginal discs to identify genes whose misexpression correlates with tumor progression
Project description:Placenta hyperplasia is commonly observed in cloned animals and is believed to impede the proper development of cloned embryos. However, the mechanism underlying this phenomenon is largely unknown. Here we show that placenta hyperplasia of cloned mouse embryos occurs in both middle and late gestation. Interestingly, restoring paternal-specific expression of an amino acid transporter Slc38a4, which loses maternal H3K27me3-dependent imprinting and becomes bi-allelically expressed in cloned placentae, rescued the overgrowth of cloned placentae at late gestation. Molecular analyses reveal that loss of Slc38a4 imprinting leads to over activation of the mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway in cloned placentae, which is likely due to the increased amino acids transportation by SLC38A4. Collectively, our study not only reveals loss of Slc38a4 imprinting is responsible for overgrowth of cloned placentae at late gestation, but also suggests the underlying mechanism involves increased amino acid transportation and over activation of mTORC1.
Project description:Meckel's and condylar cartilages are key to mandible development. In achondroplasia, the most common form of genetic dwarfism, abnormalities of these cartilages lead to micrognathia, with significant functional repercussions for affected individuals. Using cartilage laser-microdissection and RNA-seq analyses, we analyzed the genes expressed in these cartilages in a mouse model mimicking achondroplasia and compared the transcriptome of Meckel’s and condylar cartilages from E16.5 embryos of control and Fgfr3Y367C/+ mice. Over 600 genes were differentially expressed. Our data suggest that dysregulation of several pathways due to Fgfr3 gain-of function mutation constitutes an important underlying mechanism in craniofacial defects observed in achondroplasia.
Project description:To determine the effect of different mechanical stresses on protein expression in condylar cartilage, we carried out 4D label-free quantitative proteomic analysis of condylar cartilage samples from the control (CON), 0.5 mm (0.5) and 1.5 mm (1.5) groups.
Project description:Mandibular condylar cartilage (MCC) has many distinctive features reviewed in the literature, hence it would be expected that the genetic regulation of the biological process in the MCC to be different from those of other articular hyaline cartilages and epiphyseal growth cartilages. In addition, The MCC is a multi-zonal fibrocartilage containing different types of cells, which are well characterized histomorphologically, but the factors governing their morphological transition across the zones are not fully understood. Therefore, we can speculate that unique genetic profiles in vivo might exist within the four zones of MCC. We used microarrays to obtain new insights into the MCC cells by performing a comprehensive zone-specificgene expression profile analysis for each zone of the MCC isolated from 5-week-old rats using LCM technology and compare it to femoral condylar cartilage (FCC) profiles.