Project Details
Projekt
Glucocorticoids influence Schwann cell and macrophage responses in a mouse model of peripheral nerve injury (C08* (B07))
Subject Area
Molecular Biology and Physiology of Neurons and Glial Cells
Term
since 2023
Project identifier
Deutsche Forschungsgemeinschaft (DFG) - Project number 251293561
In murine hemorrhagic shock (HS) and endotoxemia, we found that impaired glucocorticoid receptor (GR) signaling exacerbates lung injury. However, COPD as a co-morbidity did not further exacerbate lung injury. Mice lacking the GR in macrophages had exacerbated lung injury, suppressed hemodynamics, and reduced survival after HS. In vitro, glucocorticoids (GCs) and β-2-adrenergic agonists synergistically activate phagocytosis of macrophages. GCs induce S1P signaling in macrophages. Following peripheral nerve injury (PNI), efficient macrophage phagocytosis is important to clear tissue debris. In addition, S1P signaling in Schwann cells (SCs) is crucial for efficient nerve regeneration. Therefore, we hypothesize that GCs influence SC and macrophage S1P-mediated responses to enhance phagocytosis and regeneration after PNI.
DFG Programme
Collaborative Research Centres
Subproject of
SFB 1149:
Danger Response, Disturbance Factors and Regenerative Potential after Acute Trauma
Applicant Institution
Universität Ulm
