Speakers - 2026

Vascular endothelial dysfunction is a key feature of many life-threatening diseases, including diabetes, atherosclerosis, cancer, and acute inflammatory conditions such as sepsis and organ injury. It is characterized by impaired vasodilation and increased vascular permeability, largely due to disruption of endothelial cell–cell junctions. These junctions—tight junctions and adherens junctions—are essential for maintaining the integrity of the endothelial barrier and are closely linked to the actin cytoskeleton. Their stability is regulated not only by structural proteins but also by intracellular signaling pathways, including cyclic adenosine monophosphate (cAMP) and small Rho GTPases.

This presentation explores the role of two actin-binding proteins, cortactin (Cttn) and adducin (Add), in regulating endothelial barrier integrity. Although these proteins have distinct functions—cortactin in actin branching and adducin in stabilizing the actin–spectrin network—both are increasingly recognized as important modulators of endothelial function. However, their precise mechanisms of action and interplay with junctional components and signaling pathways have remained unclear. Using myocardial endothelial cells derived from Cttn- and Add-knockout mice alongside wild-type controls, this study employed a range of molecular and cellular techniques, including Western blotting, ELISA, immunoprecipitation, PCR, and transendothelial electrical resistance (TEER) measurements. These approaches allowed for detailed investigation of protein expression, localization, signaling activity, and real-time barrier function.