Honors College Thesis


The Role of Syndecan-1 in Arterial Mechanotransduction. Public Deposited

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  • Hemodynamic forces regulate vascular homeostasis and arterial structure through mechanical stimuli by a process called mechanotransduction. Cellular response to mechanical forces involves coordination between cell surface receptors and intracellular signaling pathways. While previous work has focused on the role of integrin receptors in mechanotransduction, little is known about the role of cell surface proteoglycans in these processes. This work focuses specifically on the role of the cell surface proteoglycan syndecan-1 in vascular cell mechanotransduction. Mechanical forces were applied to rat aortae in an ex vivo culture system to examine the regulation of syndecan-1 expression. In addition vascular smooth muscle cells were isolated from syndecan-1 knockout mice and transfected with wild-type and mutated forms of syndecan-1 using lentiviral vectors. Wild-type, syndecan-1 knockout and transgenic human syndecan-1 mouse vascular smooth muscle cells were cultured in plates with collagen coated silicone membranes. An in vitro mechanical loading system was used to subject the cells to 1 Hz biaxial or uniaxial stretch at 10% strain at for up to two hours. We found that syndecan-1 knockout or deletion of the cytoplasmic region of syndecan-1 caused an increase in actin stress fibers and focal adhesion sites in response to mechanical strain. Further, knockout of syndecan-1 led to enhanced ERK phosphorylation in response to mechanical strain. These findings support that syndecan-1 is an important mediator of mechanotransduction in vascular cells.
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