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 hVSMC(ED) 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 (hVSMC(EX)) have a greater proliferative capacity than the hVSMC(ED) (14) In accordance with our hypotheses, the cells grown from explanted tissue did not produce TGF-β; (14).