Smooth muscle cells (SMC) are exposed to interstitial flow that imposes fluid shear stress on their surfaces (Figure 1). Enhanced interstitial flow shear stress on SMC has been shown to increase cell motility that contributes to SMC migration to the intima in atherosclerosis and intimal hyperplasia as first shown by our group (Shi et al., 2009).
Figure 1. Schematic diagrams showing interstitial flow across an artery wall exposing smooth muscle cells and fibroblasts to fluid shear stress (top), and across a tumor microvessel exposing tumor cells to fluid shear stress (bottom).
Recent work from our lab (Shi et al., 2011) has visualized a distinct surface glycocalyx layer on smooth muscle cells in vitro (Figure 2) that we have shown to be a mechanotransducer for interstitial flow shear stress on smooth muscle cells (Figure 3).
Figure 2. A confocal image of a rat aortic smooth muscle cell suspended in a collagen I gel. The surface heparan sulfate layer is stained in green and the nucleus in blue. (Figure from Qazi et al., 2013)
Figure 3. A mechanotransduction mechanism for interstitial flow shear stress on smooth muscle cells based on in vitro experiments described in Shi et al., 2011. The heparan sulfate proteoglycan (HSPG) on the surface of the cell transmits the interstitial flow shear stress to the cortical actin layer where in cooperation with integrin it leads to the phosphorylation of FAK and the enhancement of the proteolytic enzyme MMP-13 in rat (MMP-1 in human bovine or human) through transcriptional regulation. Degraded extracellular matrix facilitates enhanced cell motility.