Role of Endothelial End Binding Protein 3 (EB3) in Acute Respiratory Distress Syndrome
Session Number
2
Advisor(s)
Martin Chan PhD, Yulia Komarova PhD, Marlen Gonzales PhD Candidate
Location
A133
Discipline
Medical and Health Sciences
Start Date
15-4-2026 11:10 AM
End Date
15-4-2026 11:55 AM
Abstract
Acute Respiratory Distress Syndrome (ARDS) is a severe inflammatory lung condition characterized by disruption of the pulmonary endothelial barrier, leading to vascular leakage and respiratory failure. Although endothelial dysfunction is central to ARDS progression, the molecular regulators that maintain endothelial barrier stability during injury remain scarcely understood. This study investigates the role of End Binding Protein 3 (EB3), a microtubule-associated protein involved in cytoskeletal organization and endothelial junction regulation, in sepsis-induced lung injury. Endothelial-specific EB3 knockout mice and control mice were subjected to cecal ligation and puncture (CLP) to model ARDS. Acute lung injury was quantified using a lung scoring system to score previously stained hematoxylin and eosin (H&E) lung sections, while periodic acid-Schiff (PAS) staining was used to determine changes in surfactant levels within the lungs of endothelial EB3 knockout mice. Additionally, immunofluorescence (IF) staining was performed to examine endothelial junction integrity. By comparing lung injury and endothelial structure between control and EB3-deficient mice, this study aims to clarify the role of EB3 in endothelial barrier function and its contribution to inflammatory lung damage during ARDS
Role of Endothelial End Binding Protein 3 (EB3) in Acute Respiratory Distress Syndrome
A133
Acute Respiratory Distress Syndrome (ARDS) is a severe inflammatory lung condition characterized by disruption of the pulmonary endothelial barrier, leading to vascular leakage and respiratory failure. Although endothelial dysfunction is central to ARDS progression, the molecular regulators that maintain endothelial barrier stability during injury remain scarcely understood. This study investigates the role of End Binding Protein 3 (EB3), a microtubule-associated protein involved in cytoskeletal organization and endothelial junction regulation, in sepsis-induced lung injury. Endothelial-specific EB3 knockout mice and control mice were subjected to cecal ligation and puncture (CLP) to model ARDS. Acute lung injury was quantified using a lung scoring system to score previously stained hematoxylin and eosin (H&E) lung sections, while periodic acid-Schiff (PAS) staining was used to determine changes in surfactant levels within the lungs of endothelial EB3 knockout mice. Additionally, immunofluorescence (IF) staining was performed to examine endothelial junction integrity. By comparing lung injury and endothelial structure between control and EB3-deficient mice, this study aims to clarify the role of EB3 in endothelial barrier function and its contribution to inflammatory lung damage during ARDS