© 2002 by European Society of Cardiology
Copyright © 2002, European Society of Cardiology
Upregulation of the cytoskeletal-associated protein Moesin in the neointima of coronary arteries after balloon angioplasty: a new marker of smooth muscle cell migration?
aMedical Clinic I, University Hospital, RWTH Aachen, Pauwelsstr 30, 52074 Aachen, Germany
bInterdisciplinary Centre for Clinical Research in Biomaterials and Tissue-Material-Interaction in Implants ‘BIOMAT’, University Hospital Aachen, Pauwelsstr 30, 52074 Aachen, Germany
cDepartment for Cardio-Thoracic Surgery, University Hospital Aachen, Pauwelsstr 30, 52074 Aachen, Germany
ruediger.blindt{at}post.rwth-aachen.de
* Corresponding author. Tel.: +49-241-808-8724; fax: +49-241-888-8414
Migrating cells like coronary smooth muscle cells in restenosis change their cell shape and form cellular protrusions called filopodia. A prerequisite for filopodia formation is the rearrangement of the actin cytoskeleton. An essential role of the 78-kDa protein Moesin is described for Rho- and Rac-dependent assembly of actin filaments. In vivo Moesin is not observed in mature smooth muscle cells. The objective of this study was to demonstrate that Moesin is upregulated in migrating coronary smooth muscle cells during restenosis development. In vivo expression of Moesin was upregulated in neointimal coronary smooth muscle cells of dilated porcine coronary arteries compared to the undilated left circumflex coronary artery of the same swine. Concordant to these results Moesin expression was upregulated in migrating and invading human arterial smooth muscle cells in vitro analyzed by FACS, Western blotting and RT-PCR. In addition, the invasive potential of Moesin-positive Mel Im cells transfected with Moesin sense DNA increased by 28% as compared to mock-transfected control, whereas antisense transfected cells had a decreased invasive potential of 32%. Transfection of Moesin-negative HepG2 with Moesin sense cDNA increased the invasive potential by 43%. Finally, transfection of human arterial smooth muscle cells with Moesin sense cDNA caused an increased invasive potential of 30%. Transfection of haSMCs with antisense cDNA decreased the invasive potential by 37% in comparison to mock-transfected control. These results demonstrate for the first time an upregulation of Moesin expression in coronary smooth muscle cells of the neointima after arterial injury. The increased migrative and invasive potential of cells transfected with Moesin confirmed the functional role of Moesin in cell migration. This indicates an important role of Moesin during restenosis development.
KEYWORDS Restenosis; Angioplasty; Smooth muscle; Extracellular matrix; Cell culture/isolation
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