Líffræðifélag Íslands - biologia.is
Líffræðiráðstefnan 2025
Erindi/veggspjald / Talk/poster V52
Höfundar / Authors: Arnar Ingi Vilhjálmsson (1), Óttar Rolfsson (1, 2)
Starfsvettvangur / Affiliations: Háskóli Íslands
Kynnir / Presenter: Sonja Karoline Sigurðardóttir
Patients with shock-induced endotheliopathy (SHINE) display sustained elevations of circulating catecholamines and endothelial dysfunction, which correlate with poor outcomes and mortality. While the acute effects of catecholamines on the endothelium are well characterized, their long-term impact remains less studied. Previous work from our group has shown that catecholamines alter mitochondrial activity and protein expression in endothelial cells, highlighting mitochondria as key targets of stress responses. Preliminary data show that GRAMD1B expression increases following catecholamine stimulation. GRAMD1B is a cholesterol transport protein localized to the endoplasmic reticulum (ER), mediating cholesterol transport from the plasma membrane to the ER and implicated in ER-to-mitochondria trafficking. To investigate the role of GRAMD1B in mitochondrial function, we generated knockout endothelial cell lines, which exhibited impaired mitochondrial oxidative phosphorylation in response to catecholamine stimulation. To further examine these effects, we assessed mitochondrial structure and function using live-cell confocal microscopy with MitoTracker and JC-1. Preliminary data suggest alterations in mitochondrial morphology and membrane potential, which are being validated through quantitative analysis. Additional experiments using Filipin staining aim to define how free cholesterol distribution contributes to mitochondrial remodeling under stress.