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PhD defence: Olivia Lisa Wagman

The role of the quiescent endothelium during STING-driven inflammation and the crosstalk with endothelial metabolism

Info about event

Time

Friday 22 November 2024,  at 14:00 - 16:00

Location

The Merete Barker auditorium (1253-211), Aarhus University

On Friday 22 November at 14:00, Olivia Lisa Wagman defends her PhD dissertation entitled "The role of the quiescent endothelium during STING-driven inflammation and the crosstalk with endothelial metabolism".

Endothelial cells (ECs), which line blood vessels, are essential in regulating immune responses by facilitating the passage of immune cells from the bloodstream to infection sites. This process increases vessel permeability and requires the rearrangement of junctional proteins between ECs, the expression of adhesion markers on their surface, and the release of inflammatory molecules. Moreover, these changes often require metabolic shifts in the ECs to support their activated state.

The cGAS-STING pathway plays a critical role in regulating innate immune responses, and its dysregulation can lead to pathological conditions such as autoinflammatory diseases and cancer. In this dissertation, the role of ECs during STING-mediated inflammation was explored using different models of inflammation in vivo and assessing markers of vascular inflammatory activation. Moreover, the molecular mechanisms of endothelial STING activation were examined in vitro through genetic deletion strategies. In addition, the effects of STING activation on endothelial metabolism were studied both in vivo and in vitro using different genetic deletion strategies to explore if targeting endothelial metabolism could be a therapeutic strategy for treating STING-mediated diseases.

The summary is written by the PhD student.

The defence is public and takes place in the Merete Barker auditorium (1253-211), Aarhus University. Please see the press release for more information. 

Contact

PhD student Olivia Lisa Wagman
Mail: owag@biomed.au.dk 
Phone: 20288580

Read full press release