Project description:To investigate the regulatory role of MLO-Y4 mitochondria on chondrocytes, we isolated mitochondria from MLO-Y4 and transplanted to chondrocytes. We then performed gene expression profiling analysis using data obtained from RNA-seq of chondrocytes from vehicle group and mitochondria transplanted group.
Project description:To investigate the regulatory role of MLO-Y4 mitochondria on OA chondrocytes, we isolated mitochondria from MLO-Y4 and transplanted to chondrocytes treated with IL-1β. We then performed gene expression profiling analysis using data obtained from RNA-seq of chondrocytes from vehicle group and mitochondria transplanted group.
Project description:In this study, mitochondria were proved to be capable of delivering mitochondria to endothelial cells of transcortical blood vessel and promotes its angiogenesis. By utilizing RNA seq, we investigated the effect of osteocytes-derived mitochondria on endothelial cells.
Project description:Using oligomycin A-treated MLO-Y4 cells and primary murine aging osteocytes as a model of cells with mitochondrial dysfunction, it is demonstrated that when mitochondria are damaged, osteocytes tend to release signaling compounds including adenosine diphosphate. We identified that the nucleotide membrane receptors P2Y2 and P2Y6 transduced the ADP signal to Mfn2, a critical regulator of osteocyte mitochondrial transfer. Whole RNA sequencing (RNA-seq) analysis of mouse cortical bone showed that mitochondrial metabolism is impaired in aged osteocytes, and there are more extracellular nucleotides released into the matrix in cortical bone in aged mice as compared to that in young mice. Aging decreases expression levels of P2Y2/P2Y6 and Mfn2.