Altered Expression of Wnt Signaling Pathway Components in Osteogenesis of Mesenchymal Stem Cells in @entity571 XXXX .

@entity1 @entity571 @entity10368 @entity3546 @entity460 @entity361 @entity4149 @entity1366
INTRODUCTION: @entity571 ( @entity571 ) is characterized by altered homeostasis of joint cartilage and bone, whose functional properties rely on chondrocytes and osteoblasts, belonging to mesenchymal stem cells (MSCs). WNT signaling acts as a hub integrating and crosstalking with other signaling pathways leading to the regulation of MSC functions. The aim of this study was to evaluate the existence of a differential signaling between Healthy and @entity361 during osteogenesis. METHODS: MSCs of seven @entity571 @entity1 and six healthy controls were isolated, characterised and expanded. During in vitro osteogenesis, cells were recovered at days 1, 10 and 21. RNA and protein content was obtained. Expression of WNT pathway genes was evaluated using RT-qPCR. Functional studies were also performed to study the MSC osteogenic commitment and functional and post-traslational status of @entity3546 and several receptor @entity4149 kinases. RESULTS: Several genes were downregulated in @entity361 during osteogenesis in vitro. These included soluble Wnts, inhibitors, receptors, co-receptors, several kinases and transcription factors. Basal levels of @entity3546 were higher in @entity361 , but @entity460 deposition and expression of osteogenic genes was similar between Healthy and @entity361 . Interestingly an increased phosphorylation of @entity10368 /42 MAPK ( @entity1366 ) signaling node was present in @entity361 . CONCLUSION: Our results point to the existence in @entity361 of alterations in expression of Wnt pathway components during in vitro osteogenesis that are partially compensated by post-translational mechanisms modulating the function of other pathways. We also point the relevance of other signaling pathways in @entity571 pathophysiology suggesting their role in the maintenance of joint homeostasis through modulation of MSC osteogenic potential.
