A 3D Arterial Organoid System for Modeling Atherosclerosis Mechanisms and Inflammatory Responses
Molloy Faculty Mentor
Dr. Jodi F. Evans
Presenter Major
Biology
Presentation Type
Poster
Location
Wilbur 2nd Floor Corridor, Wilbur Arts Building, Molloy University
Start Date
1-5-2026 10:30 AM
End Date
1-5-2026 11:15 AM
Description (Abstract)
The National Institutes of Health announced an initiative to reduce animal use in medical research while expanding human-based in vitro systems such as organoids. In alignment with this effort, we developed a 3D arterial organoid model to investigate mechanisms contributing to atherosclerosis, a leading cause of morbidity worldwide. Vascular smooth muscle cells were embedded within a collagen matrix and layered with endothelial cells to form an arterial construct. Fluorescently labeled macrophages were introduced, and constructs were treated with LDL in the presence or absence of leptin to emulate inflammation. Following treatment, conditioned medium was collected for analysis, and constructs were processed for histological and fluorescence imaging. Staining confirmed structural integrity, and microscopy demonstrated macrophage invasion. Analysis of inflammatory markers revealed reduced nitric oxide production with elevated LDL and increased TNFα production with leptin exposure. These findings support the model’s ability to replicate inflammatory features and its potential for therapeutic investigation.
Keywords
Organoid, Atherosclerosis, Leptin, In-vitro, LDL
Related Pillar(s)
Study
A 3D Arterial Organoid System for Modeling Atherosclerosis Mechanisms and Inflammatory Responses
Wilbur 2nd Floor Corridor, Wilbur Arts Building, Molloy University
The National Institutes of Health announced an initiative to reduce animal use in medical research while expanding human-based in vitro systems such as organoids. In alignment with this effort, we developed a 3D arterial organoid model to investigate mechanisms contributing to atherosclerosis, a leading cause of morbidity worldwide. Vascular smooth muscle cells were embedded within a collagen matrix and layered with endothelial cells to form an arterial construct. Fluorescently labeled macrophages were introduced, and constructs were treated with LDL in the presence or absence of leptin to emulate inflammation. Following treatment, conditioned medium was collected for analysis, and constructs were processed for histological and fluorescence imaging. Staining confirmed structural integrity, and microscopy demonstrated macrophage invasion. Analysis of inflammatory markers revealed reduced nitric oxide production with elevated LDL and increased TNFα production with leptin exposure. These findings support the model’s ability to replicate inflammatory features and its potential for therapeutic investigation.
