Abstract
Migration of vascular smooth muscle cells (VSMCs) from the media to intima constitutes a critical step in the development of proliferative vascular diseases. To elucidate the regulatory mechanism of VSMCs motility, the roles of caldesmon (CaD) were investigated previously. CaD is an actin-binding protein dynamically regulating cytoskeleton structure. In this study, the potential role of CaD in mediating proliferation and motility of VSMCs were discussed. First, structural effect of CaD on cytoskeleton integrity was analyzed with CaD knock-down; second, the proliferation of VSMCs was measured in CaD knock-down and control cells; third, the specific role of CaD on VSMCs motilities was evaluated with in vitro migration and invasion assays. We found that CaD is an integral component to maintain cytoskeleton integrity of VSMCs. Our data indicated that CaD suppression does not show significant influence on VSMCs proliferation, but negatively modulates the motilities of VSMCs, and CaD depletion would significantly facilitate migration and invasion of VSMCs.
Highlights
Migration of vascular smooth muscle cells (VSMCs) from media to intima is a critical step in the development of proliferative vascular diseases such as atherosclerosis, and in response to vascular injuries such as angioplasty and organ transplantation [1] [2]
The Influence of CaD Suppression on Cytoskeleton Integrity of Dedifferentiated VSMCs To evaluate how CaD affects the structure of cytoskeleton in primary VSMCs, we used CaD shRNA lentiviral particles to stably knock down CaD expression in human aortic smooth muscle cells (HASMCs), the lentiviral particles packed with scrambled shRNA sequence were employed as control
When we explored the basic function of CaD in cytoskeleton stability of HASMCs, we found actin filaments were promptly disrupted in CaD depleted cells, only short-thin stress fibers could be detected in the area of membrane ruffles and lamellipodial extensions, whereas the control cells showed very robust cytoskeleton bundling crossing the entire cytoplasm with long-strong stress fibers (Figure 2), these results are very consistent with the previous studies that depleting CaD by gene silencing impairs stress fibers in non-muscle cells [16], which may suggest CaD is a critical element for the formation of thick stress fibers in primary cultured dedifferentiated VSMCs
Summary
Migration of vascular smooth muscle cells (VSMCs) from media to intima is a critical step in the development of proliferative vascular diseases such as atherosclerosis, and in response to vascular injuries such as angioplasty and organ transplantation [1] [2]. Differentiated VSMCs normally do not proliferate or migrate. How to cite this paper: Gao, B. and Jiang, Q.F. (2016) The Influence of Caldesmon Suppression on Proliferation and Motilities of Vascular Smooth Muscle Cells. J. Biomedical Science and Engineering, 9, 430-436.
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