A significant determinant of atherosclerosis has been identified in the inflammatory signalling produced from the activation of Lectin-like oxidized low-density lipoprotein (LDL) receptor-1 (LOX-1) by its cognate ligand, oxidised LDL (OxLDL) (1). Recent studies support the idea that G protein-coupled receptors (GPCRs) form heteromers with, and transactivate, non-GPCR partner receptors to cause varying changes to their pharmacology, signalling and intracellular trafficking (2). Of interest is the idea that LOX-1 can form heteromeric complexes with GPCRs, such as angiotensin II type 1 (AT1) receptor (3). These may lead to a plethora of changes to receptor pharmacology and an upregulation in inflammatory signalling, contributing to atherosclerotic outcomes.
The present study aimed to investigate interactions between LOX-1 and the AT1 receptor, using the Receptor-Heteromer Investigation Technology (Receptor-HIT) (4) assay in HEK293FT cells. Receptor-HIT detects receptor heteromers through the ligand-induced recruitment of interacting proteins to the heteromer, using a proximity-based biophysical technique such as bioluminescence resonance energy transfer (BRET) (5). By co-expressing one luciferase-labelled receptor and one unlabelled receptor, as well as a fluorophore-labelled interacting protein, Receptor-HIT detects a BRET signal upon treatment with a ligand specific for the unlabelled receptor. This indicates recruitment of the interacting protein to the receptor heteromer, which may provide insights into pharmacological changes such as with G protein-signalling.
It was found that LOX-1 produced Receptor-HIT signals indicative of heteromerisation when co-transfected with the AT1 receptor and various signalling proteins. Additionally, AT1 and LOX-1 co-transfection selectively altered some of the downstream signalling properties of the receptors. These findings support the existence of the AT1-LOX-1 heteromer and provide evidence of novel pharmacological changes which may be related to atherosclerosis pathogenesis.