My overall research has focussed on the regulatory role of the cytokine vascular endothelial growth factor A (VEGF) in endothelial cells (ECs), in physiological and pathological conditions. During my PhD, I worked with endothelial progenitor cells (EPCs) harvested from human volunteers and discovered that VEGF-induced calcium (Ca2+) signals trigger the molecular mechanisms that drive EPC proliferation and tubulogenesis in the healthy adult. Further, I discovered that such pathways are altered in EPCs harvested from the peripheral blood of cancer patients. These contributions not only increased the understanding of Ca2+ signalling in EPCs, but also indicated novel potential targets for therapy. As a post-doc, my research has been focused on two different topics: 1) the process of lymphocyte migration across ECs of the blood-brain barrier and 2) the mechanisms by which VEGF and the pro-inflammatory peptide bradykinin induce permeability of retinal blood vessels. To measure real-time changes of endothelial permeability and signalling in intact retinal blood vessels, I established an ex-vivo model of vascular leakage using mouse retinas. 

Thereby I uncovered a phosphorylation cascade that links VEGF and bradykinin to the activation of AMPK, a protein kinase not previously associated with vascular leakage in the retina. My research showed that AMPK is a key mediator of VEGF- and bradykinin-induced vascular leakage downstream of Ca2+ signalling and upstream of eNOS signalling, to the junctional adhesion molecule vascular endothelial cadherin. Moreover, AMPK is upstream of the p38 stress kinase and the heath shock protein HSP27, which regulate actin rearrangement of the cells. My work, therefore, links three different signalling pathways into one signalling network that is activated by both VEGF and bradykinin. 

I then joined the lab of Prof. Christiana Ruhrberg, where I am now defining the role of the transmembrane protein neuropilin 1 (NRP1) in retinal ECs. 

My plan is to build on all the expertise I have acquired on Ca2+ signalling, endothelial cells, and retinal physiology to establish a research group that investigates how Ca2+ signals regulate the retinal vasculature in physiological conditions and how Ca2+ signals are dysregulated in retinal disease.