Abstract

See article by Jalvy et al. [8] (pages 738–747) in this issue . Cell migration might be considered one of the most basic requirements in vascular development and one of the most basic problems in vascular disease. Recruitment of precursors to vascular smooth muscle cells (SMC) is essential for the formation of vascular media in embryonic development [1], but it also fuels the growth of atherosclerotic plaques and neointimal hyperplasia after angioplasty [2,3]. Conversely, lack of recruitment of SMC precursor cells may contribute to arterio-venous malformations in hereditary hemorrhagic telangiectasia [4]. Lack of pericytes, often considered to be the SMC correlate in the microvasculature, causes defective microvascular homeostasis [5]. The platelet-derived growth factor (PDGF), in particular PDGF-BB, is recognized as a key factor for SMC migration and proliferation [6]. As such, it is essential for the formation of the vascular wall, and deletion of the PDGF-B gene results in … * Division of Cardiology, David Geffen School of Medicine at UCLA, Box 951679, Los Angeles, CA 90095-1679, United States. Tel.: +1 310 794 4417; fax: +1 310 2068553. kbostrom{at}mednet.ucla.edu

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