Abnormal proliferation of human vascular smooth muscle cells (hVSMCs) is a central event in the development of atherosclerosis (1 –3 ) As a result, there is considerable interest in the establishment of hVSMC cultures as a mode1 of this disease process However, it has been noted in the past (4 ,5 ) that hVSMCs, especially when cultured by the enzyme-dispersal technique (hVSMC,ED ), grow poorly in culture compared to VSMCs from other species (e.g., rat) This has limited their use for cell-culture studies. We have recently reported that the reduced proliferative capacity of hVSMCED from adult aorta can be attributed to the endogenous production of active TGF-β(6 ,7 ). We (6 –8 ) and others (9 –11 ) have shown that TGF-β; is a potent inhibtior of smooth muscle cell proliferation. Moreover, recent studies in animal models of atherosclerosis (12 ) have suggested that TGF-P plays a pivotal role in regulation of vessel wall architecture (13 ). We have also shown that hVSMCs derived by the alternative method of explanting (hVSMCEX ) have a greater proliferative capacity than the hVSMCED (14 ) In accordance with our hypotheses, the cells grown from explanted tissue did not produce TGF-β; (14 ).
