Our research is directed at how cell death features (type, timing, extent) govern the type of regenerative strategy employed by a biological system.
We primarily use the murine pancreas as a model system, due to the wide-range of genetic tools available for this organ and its demonstrated cell plasticity potential. Besides employing classical systems of rapid cell-ablation (RIP-DTR, chemical ablation), we developed novel transgenic models of progressive β-cell decay (financed by Excellence Project for Young Investigators of Novo Nordisk Foundation). By coupling the diverse β-cell ablation configurations with genetic cell tracing, timed conditional gene expression and diverse omics assays, we study the dynamical molecular fingerprint of β-cell death and the regenerative response employed, with focus on β-cell self-renewal potential (financed by FRIPRO Young Research Talent grant – Research Council of Norway).
- (2021). Chronically elevated exogenous glucose elicits antipodal effects on the proteome signature of differentiating human ipsc-derived pancreatic progenitors. International Journal of Molecular Sciences.
- (2020). In vivo environment swiftly restricts human pancreatic progenitors toward mono-hormonal identity via a HNF1A/HNF4A mechanism. Frontiers in Cell and Developmental Biology. 1-14.
- (2019). In vivo hyperglycemia exposure elicits distinct period-dependent effects on human pancreatic progenitor differentiation, conveyed by oxidative stress. Acta Physiologica. 1-16.