Líffræðifélag Íslands - biologia.is
Líffræðiráðstefnan 2025
Erindi/veggspjald / Talk/poster E55
Höfundar / Authors: Arnar Ingi Vilhjálmsson* (1), Eva Jacobsen (1), Óttar Rolfsson (1)
Starfsvettvangur / Affiliations: Háskóli Íslands (1)
Kynnir / Presenter: Arnar Ingi Vilhjálmsson
Patients with shock-induced endotheliopathy (SHINE) display sustained elevations of circulating catecholamines and endothelial dysfunction, which correlate with poor outcomes and mortality. Using an in vitro endothelial model, catecholamine treatment induced expression of GRAMD1B, a cholesterol transport protein that regulates intracellular lipid homeostasis. However, its role in endothelial biology remains poorly defined. To investigate this, we generated a GRAMD1B knockout endothelial cell line. Loss of GRAMD1B disrupted cholesterol handling and lipid homeostasis, impaired proliferation, and induced a stressed phenotype marked by increased expression of endothelial dysfunction markers. GRAMD1B-deficient cells also displayed altered angiogenic activity and reduced mitochondrial oxidative phosphorylation following adrenergic stimulation. Together, these findings identify GRAMD1B as an important regulator of endothelial stress adaptation, linking cholesterol trafficking to mitochondrial function and angiogenic behavior relevant to endothelial dysfunction.