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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:1246.)
© 2006 American Heart Association, Inc.

Brief Reviews

Modulation of Smooth Muscle Cell Migration by Members of the Low-Density Lipoprotein Receptor Family

Hideaki Bujo; Yasushi Saito

From the Departments of Genome Research and Clinical Application (H.B.), and Clinical Cell Biology (Y.S.), Chiba University Graduate School of Medicine, Japan.

Correspondence to Hideaki Bujo; Department of Genome Research and Clinical Application, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan. E-mail hbujo{at}faculty.chiba-u.jp

Low-density lipoprotein receptor family members (LRs) play a key role in the catabolism of many membrane-associated proteins, such as complexes between proteinases and their receptors, in addition to being involved in lipoprotein metabolism as suspected by the hitherto well-established functions of low-density lipoprotein receptor, in a variety of tissues. Recent studies using receptor-deficient or -overexpressing animals and cells have suggested that certain LRs are important regulators of the migration (and proliferation) of vascular smooth muscle cells (SMCs). LR expression is markedly induced in intimal or medial SMCs during the formation of atherosclerotic lesions. Because LRs can modulate the activity of the urokinase-type plasminogen activator (uPA) receptor and possibly of the platelet-derived growth factor (PDGF) receptor, LRs may influence the migration of SMCs through functional modulation of these membrane receptors. Therefore, SMC migration may be regulated by time-restricted expression of LRs. In agreement with the concept of functional interaction between LRs and membrane signaling receptors, a negative regulator of uPA receptor protein catabolism, LR11, has been identified. Statins modulate the PDGF-induced migration of intimal SMCs via the LR11/uPA receptor cascade. Selective modification of the LRs/uPA receptor/PDGF receptor systems in SMCs may be important for suppression of atherosclerotic plaque formation as well as for preventing intimal thickening after angioplasty.

LDL receptor family members (LRs) regulate the catabolism of membrane-associated proteins and are expressed in SMCs of atherosclerostic lesions. LRs modulate the activity of the urokinase-type plasminogen activator (uPA) receptor and possibly of the PDGF receptor. Selective modification of the LRs/membrane receptor system may be important for suppression of atherosclerosis.

Key Words: LDL receptor family • smooth muscle cells • migration • LR11 • urokinase-type plasminogen activator receptor • PDGF receptor

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