Viviane Fleischhacker, Filip Milosic, Marko Bricelj, Kristina Kührer, Katharina Wahl-Figlash, Patrick Heimel, Andreas Diendorfer, Eleonora Nardini, Irmgard Fischer, Herbert Stangl, Peter Pietschmann, Matthias Hackl, Roland Foisner, Johannes Grillari, Markus Hengstschläger, Selma Osmanagic-Myers
Age-induced decline in osteogenic potential of bone marrow mesenchymal stem cells (BMSCs) potentiates osteoporosis and increases the risk for bone fractures. Despite epidemiology studies reporting concurrent development of vascular and bone diseases in the elderly, the underlying mechanisms for the vascular-bone cross-talk in aging are largely unknown. In this study, we show that accelerated endothelial aging deteriorates bone tissue through paracrine repression of Wnt-driven-axis in BMSCs. Here, we utilize physiologically aged mice in conjunction with our transgenic endothelial progeria mouse model (Hutchinson-Gilford progeria syndrome; HGPS) that displays hallmarks of an aged bone marrow vascular niche...
April 5, 2024: Aging Cell