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Access Type
WSU Access
Date of Award
January 2022
Degree Type
Thesis
Degree Name
M.S.
Department
Molecular Biology and Genetics
First Advisor
Li Li
Abstract
A life-threatening clinical manifestation of Marfan Syndrome (MFS) is the development of thoracic aortic aneurysms (TAA) which can lead to dissection and or rupture. MFS is caused by mutations in extracellular matrix (ECM) protein, Fibrillin-1 (FBN1) which forms the structural component of elastic microfibrils. It is unclear how mutations in FBN1 cause aneurysm development and progression. In recent years, inflammation and immune cells are being considered an important biological process that contributes to TAA. However, the exact roles of the immune cells are unknown. Here we find increased CD11b+ cells recruited and infiltrated into the vessel wall and their spatial distribution suggesting that innate immune signaling plays in important role in aneurysm progression. The presence of p47phox expression to one area of the vessel wall and the expression of superoxide dismutase 1 (SOD1) shows reactive oxygen species (ROS) are present. Increased MMP9 expression is also correlated with increased CD11b expression suggest a correlation with immune cells contributing to further ECM degeneration. This phenomenon is correlated with the size of the dilation and is expressed the highest in the very late stage of aneurysm. These findings prompt the inhibition of CD11b+ cells infiltration to the vessel wall in our aneurysm mouse model to evaluate the survival curve and integrity of the vessel wall to elucidate more the roles these cells play in rupture of aneurysm. The results from future studies will reveal potential therapeutic targets to manage TAA progression.
Recommended Citation
Pham, Lucynda, "Increased Cd11b+ Immune Cells Contribute To Thoracic Aortic Aneurysm Rupture" (2022). Wayne State University Theses. 873.
https://digitalcommons.wayne.edu/oa_theses/873