Welcome to the Pröschel Lab
Within the context of our work on glial progenitor cells, we are now focusing on the role of astrocytes as critical modulators in response to injury or stress. The importance of understanding this process is emphasized by our discovery that the generation of mature astrocytes may be impaired in Vanishing White Matter leukodystrophy (Nat Med. 2005 Mar;11(3):277-83.).
The ability to study astrocyte development in normal and pathological conditions, provides a unique opportunity to test the utility of glial precursor cells and their astrocytic progeny for cell transplantation therapy in diseases of the central nervous system (CNS), such as traumatic injury (spinal cord and traumatic brain injury) and neurodegenerative diseases (Parkinsons Disease, Multiple sclerosis).
We have identified distinct astrocyte populations that demonstrate different functional properties with respect to their ability to promote injury repair upon transplantation into the injured nervous system. While one type shows little benefit and may even cause neuropathic pain syndrome, the other remodels the injured host tissue, enables axon outgrowth and extensive functional recovery (J Biol 2006 Apr 27, 5(3):7; J Biol 2008 Sep 19;7(7):245). As a prerequisite for the transition to the clinic we are analyzing the factors secreted by these astrocytes and have now derived homologous astrocyte populations from human precursor cells. (PLoS One. 2011 Mar 2;6(3)).
Current Research Projects
- A novel mouse model for ataxia-telangiectasia with a N-terminal mutation displays a behavioral defect and a low incidence of lymphoma but no increased oxidative burden.Hum Mol Genet. 24, 6331-49. (2015 Nov 15).
- Mutation of ataxia-telangiectasia mutated is associated with dysfunctional glutathione homeostasis in cerebellar astroglia.Glia. (2015 Oct 15).
- Redox biology in normal cells and cancer: restoring function of the redox/Fyn/c-Cbl pathway in cancer cells offers new approaches to cancer treatment.Free Radic Biol Med. 79, 300-23. (2015 Feb 01).