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Characterizing the role of myeloid-specific heme oxygenase-1 (HO-1) in the regulation of circadian rhythmicity, neuroinflammation and neuronal injury following brain trauma

Subject Area Anaesthesiology
Term from 2017 to 2024
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 398425865
 
Final Report Year 2024

Final Report Abstract

In this two-part project, we first describe how the HO-1/CO (heme oxygenase 1; carbon monoxide) system interacts with mechanisms controlling circadian rhythm to determine the extent of neuronal injury after hemorrhagic stroke. We employed both in vitro and in vivo studies to demonstrate that the presence of HO-1 specifically in microglia directly influences the expression of circadian control genes and that changes in the circadian gene expression profile are linked to processes critical to injury response after hemorrhage, such as CD36-mediated erythrophagocytosis and the neuroinflammatory response. Additional human observational data link both circadian control genes and HO-1 to functional neurological outcome and delirium, providing evidence for the clinical relevance of these pathways and for their potential use as prognostic markers in traumatic and hemorrhagic brain injury. We continue to provide evidence for a delicate circadian crosstalk via direct neural interaction between peripheral organs such as the kidney and the central nervous system that might influence susceptibility to injury of both the brain after hemorrhage and peripheral organs. In the second part of this project, we start with a characterization of the reactive transformation of astrocytic glial cells in response to traumatic brain injury and demomstrate that the presence of HO-1 specifically in microglia critically influences the transformation towards harmful vs. protective astrocytic polarization. Furthermore, in vitro, in vivo and correlative human data demontrate a differential role of microglial and astrocytic HO-1 in determining neuroinflammation and neuronal injury after head trauma, with HO-1-specific changes in glial cell activation, cytokine production, Tolllike receptor (TLR) expression and ultimately neuronal damage after traumatic injury. Collectively, these results provide further insight into the pathophysiology of neuronal damage after hemorrhagic and traumatic brain injury and how interference with HO-1 and circadian control might be associated with improved neurological outcome. They demand further basic science and clinical investigations studying the potential neuroprotective properties of interaction with these physiological systems.

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