Annals of biomedical engineering · 2026
Murine Abdominal Aortic Aneurysm Intraluminal Thrombus Composition and Structure.
СтатьяНазвание и аннотация: Перевод в очереди
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Johns Cortland H, Schepers Luke E, Foist Annabelle M F, Foster Ethan P, Bedi Anish, Narra Niharika, Albrecht Claudia K, Cox Abigail D, Goergen Craig J
Аннотация
PURPOSE: Many abdominal aortic aneurysm (AAA) patients develop intraluminal thrombus (ILT), but the role of ILT in AAA progression and rupture is poorly understood.
METHODS: To evaluate ILT in AAAs, we induced AAAs in C57Bl6/J mice via surgical application of topical elastase to the abdominal aorta below the renal arteries and administration of β-aminopropionitrile (BAPN) in drinking water. Ultrasound images of these AAAs were collected longitudinally over a period of 56 days to evaluate AAA growth over time. We semi-quantitatively assessed elastin degradation and inflammation from Movat's pentachrome and H&E-stained samples, respectively. Additionally, we assessed extracellular matrix composition and elastin quality through Movat's pentachrome stained samples.
RESULTS: Mice subjected to elastase + BAPN exhibited continuous and significant AAA growth over time. Mice with ILT had more significant expansion over the length of the study (p < 0.05). From histology, ILT samples showed more elastin damage, greater collagen and proteoglycan accumulation, and greater inflammation than aneurysms without ILT. From scanning electron microscopy, we confirmed the presence of fibrin sheets and abnormally shaped red blood cells (polyhedrocytes) within ILT. We also observed that tissue samples with greater inflammation were correlated with more elastin damage. Increased aortic expansion and wall damage may create hemodynamic conditions conducive to initiation of ILT deposition: endothelial damage and reduced blood flow.
CONCLUSION: Understanding the relationship between ILT formation, aortic wall degradation, and inflammation could help refine clinical strategies for monitoring and treating AAAs. These data suggest that work focused on modulating inflammation and ILT formation could offer promising pathways for non-surgical intervention in AAA treatment.
METHODS: To evaluate ILT in AAAs, we induced AAAs in C57Bl6/J mice via surgical application of topical elastase to the abdominal aorta below the renal arteries and administration of β-aminopropionitrile (BAPN) in drinking water. Ultrasound images of these AAAs were collected longitudinally over a period of 56 days to evaluate AAA growth over time. We semi-quantitatively assessed elastin degradation and inflammation from Movat's pentachrome and H&E-stained samples, respectively. Additionally, we assessed extracellular matrix composition and elastin quality through Movat's pentachrome stained samples.
RESULTS: Mice subjected to elastase + BAPN exhibited continuous and significant AAA growth over time. Mice with ILT had more significant expansion over the length of the study (p < 0.05). From histology, ILT samples showed more elastin damage, greater collagen and proteoglycan accumulation, and greater inflammation than aneurysms without ILT. From scanning electron microscopy, we confirmed the presence of fibrin sheets and abnormally shaped red blood cells (polyhedrocytes) within ILT. We also observed that tissue samples with greater inflammation were correlated with more elastin damage. Increased aortic expansion and wall damage may create hemodynamic conditions conducive to initiation of ILT deposition: endothelial damage and reduced blood flow.
CONCLUSION: Understanding the relationship between ILT formation, aortic wall degradation, and inflammation could help refine clinical strategies for monitoring and treating AAAs. These data suggest that work focused on modulating inflammation and ILT formation could offer promising pathways for non-surgical intervention in AAA treatment.