nanoGe - CellMatrix - Beta-sarcoglycan deficiency displays reduced atherosclerotic plaque development in ApoE-null mice

Beta-sarcoglycan deficiency displays reduced atherosclerotic plaque development in ApoE-null mice

Uwe Rauch^a, Anna Hultgardh Nilsson^a, Vignesh Murugesan^a

^aDepartment of Experimental Medical Science, Lund University, Sweden, Sölvegatan 19, 221 84 Lund, Sweden

Proceedings of New Advances in Probing Cell-ECM Interactions (CellMatrix)

Berlin, Germany, 2016 October 20th - 21st

Organizers: Ovijit Chaudhuri, Allen Liu and Sapun Parekh

Poster, Vignesh Murugesan, 012
Publication date: 25th July 2016

Introduction Beta-sarcoglycan (β-SG), a transmembrane protein and component of the sarcoglycan complex, is part of the Dystrophin-glycoprotein complex (DGC). The DGC connects the actin cytoskeleton of smooth muscle cells to the basement membrane. Perturbation or removal of β-SG can lead to loss of the entire sarcoglycan complex and subsequent de-stabilization of the DGC. During atherosclerotic plaque development, vascular smooth muscle cells change their phenotype from a contractile to a synthetic and begin synthesizing different or altered connective tissue molecules and take part in the deposition of ECM proteins in plaques. Here we aim to determine the role of β-SG in the development of atherosclerosis. Methods & Results In our model of restenotic-type plaques formed due to collar induced injury, we observe a β-SG -/- phenotype which mimics that seen in our previous study with dystrophin (mdx) mutated model. Although β-SG and dystrophin are part of the same DGC complex, the absence of β-SG has an effect extracellularly whilst dystrophin intracellularly. In a shear stress model, inflammatory plaques were formed in the carotid artery of mice with the lipid transport regulator ApoE removed and under a high fat diet. In the β-SG model, similar to results seen in mdx model, a reduction in plaque size and an increase in marker for differentiated SMC's (Myosin heavy chain 11) are observed. In accordance with the plaque size reduction, total plaque burden were also nearly significantly reduced (P=0.055, measured by flat preparation of aortas with Oil red O- staining). The T cell marker CD3+ was shown to be involved in formation of plaques previously in the mdx ApoE model, we were unable to detect any difference in CD3+ expression in β-SG ApoE plaques. Here we show a significant role of beta-sarcoglycan in plaque development; further investigation into mechanism underlying these observations are yet to be elucidated.

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