Denise Jahn, Paul Richard Knapstein, Ellen Otto, Paul Köhli, Jan Sevecke, Frank Graef, Christine Graffmann, Melanie Fuchs, Shan Jiang, Mayla Rickert, Cordula Erdmann, Jessika Appelt, Lawik Revend, Quin Küttner, Jason Witte, Adibeh Rahmani, Georg Duda, Weixin Xie, Antonia Donat, Thorsten Schinke, Andranik Ivanov, Mireille Ngokingha Tchouto, Dieter Beule, Karl-Heinz Frosch, Anke Baranowsky, Serafeim Tsitsilonis, Johannes Keller
Traumatic brain injury (TBI) leads to skeletal changes, including bone loss in the unfractured skeleton, and paradoxically accelerates healing of bone fractures; however, the mechanisms remain unclear. TBI is associated with a hyperadrenergic state characterized by increased norepinephrine release. Here, we identified the β2 -adrenergic receptor (ADRB2) as a mediator of skeletal changes in response to increased norepinephrine. In a murine model of femoral osteotomy combined with cortical impact brain injury, TBI was associated with ADRB2-dependent enhanced fracture healing compared with osteotomy alone...
April 17, 2024: Science Translational Medicine