Dresden International Graduate School for Biomedicine and Bioengineering

The research group focusses on adult stem cells of the hypothalamus-pituitary-adrenocortical (HPA) axis and their role in restraint and metabolic stress.

Recently, we have identified a novel progenitor population in the adrenal cortex. Under normal homeostasis this Nestin-positive cell population is quiescent but under different forms of stress, we have shown an increase in migration and differentiation into steroid-producing cells.

An imbalance of the stress response has been strongly associated with various health conditions. These include mental disorders such as major depression, anxiety disorders, burnout and somatic manifestations such as dermatitis, and metabolic disorders. Our results indicate that an early sensitization of stem cells of the HPA-axis leading to epigenetic changes might be responsible for this increased risk of developing mental disorders in adulthood. Therefore, we are investigating what happens to stem cells under stress and which signal pathways are involved in the stress response by using animal stress models, RT-qPCR, transcriptomic, proteomic and lipodomic approaches.

In vitro, we are able to isolate these stem cells/ progenitors and differentiate them into steroid-producing cells. The long-term goal is to use such cells for regenerative therapies in order to treat diseases such as adrenal insufficiency.

Last year, we started a second project investigating the impact of metabolic diseases on COVID-19. Metabolic diseases are associated with an increased risk of severe COVID-19 and conversely, new-onset hyperglycemia and complications of preexisting diabetes have been observed in COVID-19 patients. Analyzing pancreatic autopsy tissue from COVID-19 patients using immunofluorescence, immunohistochemistry, RNA scope and electron microscopy, we detected SARS-CoV-2 viral infiltration of beta-cells in all patients. Using SARS-CoV-2 pseudoviruses, we confirmed that isolated human islet cells are permissive to infection. Even in the absence of manifest new-onset diabetes, necroptotic cell death, immune cell infiltration and SARS-CoV-2 viral infection of pancreatic beta-cells may contribute to varying degrees of metabolic dysregulation in patients with COVID-19.