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Takahashi, M., Hayashi, K., Yoshida, K., Ohkawa, Y., Komurasaki, T., Kitabatake, A., et al. (2003) Epiregulin as a Major Autocrine/Paracrine Factor Released from ERK and p38MAPK-Activated Vascular Smooth Muscle Cells. Circulation, 108, 2524-2529.
http://dx.doi.org/10.1161/01.cir.0000096482.02567.8c

has been cited by the following article:

• TITLE: The Influence of Caldesmon Suppression on Proliferation and Motilities of Vascular Smooth Muscle Cells

  AUTHORS: Bin Gao, Qifeng Jiang

  KEYWORDS: Caldesmon, Proliferation, Motility, VSMCs

  JOURNAL NAME: Journal of Biomedical Science and Engineering, Vol.9 No.9, August 12, 2016

  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.