The `response to retention hypothesis of atherogenesis proposes that proteoglycans bind and retain low-density lipoproteins (LDL) in the vessel wall. Platelet-derived growth factor (PDGF) is strongly implicated in atherosclerosis and stimulates proteoglycan synthesis. Here we investigated the action of the PDGF receptor inhibitor imatinib on PDGF-mediated proteoglycan biosynthesis in vitro, lipid deposition in the aortic wall in vivo and the carotid artery ex vivo. In human vSMCs, imatinib inhibited PDGF mediated 35S-SO4 incorporation into proteoglycans by 31 (P <0.01) and inhibited PDGF-mediated size increases in both chemically cleaved and xyloside associated glycosaminoglycan (GAG) chains by 19 , P <0.05 and 27 , P <0.05, respectively.
Ballinger, M. L., Osman, N., Hashimura, K., De Haan, J. B., Jandeleit-Dahm, K. A., Ilen, T. A., Tannock, L., Rutledge, J. C., & Little, P. J. (2010). Imatinib inhibits vascular smooth muscle proteoglycan synthesis and reduces LDL binding in vitro and aortic lipid deposition in vivo. Journal of Cellular and Molecular Medicine, 14(6B), 1408 - 1418. https://doi.org/10.1111/j.1582-4934.2009.00902.x.