Laboratory of gene expression regulation in neural stem cells

Dr. Carlos P. Fitzsimons


The Fitzsimons lab studies the regulation of gene expression in neural stem cells. Within this frame we focus on regulation by (ligand activated) transcription factors, such as hormone receptors, and microRNAs. In particular, we study the effect that brain insults such as physical or psychological stress, epileptic seizures, traumatic brain injury and others may have on adult neural stem cells in the hippocampus and how they are associated with neurodegeneration.

Within the REACT NSC consortium we investigate the changes induced by traumatic brain injury in hippocampal neural stem cells and neural stem cell-derived reactive astrocytes at the transcriptional, posttranscriptional and protein levels. One of the central aims here is to understand to what extent reactive astrocytes generated from preexisting astrocytes differ from those generated from reactive neural stem cells.

Further, we contribute confocal microscopy, super-resolution microscopy and cell quantification techniques to quantitatively analyze specific cell populations, their identity proliferation and differentiation, which are used within the REACT NSC consortium to characterize neural stem cell fate decisions after traumatic brain injury.

Finally, we aim to understand how particular microRNAs and other specific regulators of gene expression contribute, and may be used to revert, the activation of neural stem cells and the production of reactive neural stem cells after traumatic brain injury.

Techniques

We use a “multi-omics” approach based on transcriptomics, proteomics and microRNAs profiling techniques that allows us to characterize specific gene expression profiles in neural stem cells, associated with traumatic brain injury.

We complement this multi-omics approach with super-resolution microscopy techniques to understand how specific gene expression profiles can be linked to particular cell states in specific neural stem cell populations after traumatic brain injury.