Abstract
Proliferation and migration of vascular smooth muscle cells (VSMCs) are involved in the processes of atherosclerosis and restenosis. The protein product of the growth arrest-specific gene 6 (Gas-6) has recently been identified as a ligand for the Axl/Rse/ Mer tyrosine kinase receptor family, which may be involved in proliferation and migration of VSMCs. Here we show that Gas-6 gene expression is increased in proliferating VSMCs in tissue culture (2.5-fold increase by Northern blot) and following neointimal proliferation in a rabbit balloon-injury model (3-fold increase by Western blot). Neither platelet-derived growth factor (PDGF) nor thrombin stimulate the expression of Gas-6 in cultured VSMCs despite the ability of the PDGF, but not thrombin, to stimulate proliferation in growth-arrested cells. These data suggest a role for the Gas-6 regulatory system in VSMC proliferation, which may be a target for therapeutic interventions in the atherosclerotic process and restenosis after angioplasty.
Original language | English |
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Pages (from-to) | 3851-3856 |
Number of pages | 6 |
Journal | Electrophoresis |
Volume | 21 |
Issue number | 17 |
DOIs | |
Publication status | Published - 18 Dec 2000 |
Externally published | Yes |
Keywords
- Balloon-injury model
- Gas-6
- Platelet-derived growth factor
- Thrombin
- Vascular smooth muscle cells