Rele of the interaction between arterial smooth muscle cellsand endothelial cell or macrophages in foam cell formation.

1巨噬细胞与平滑肌细胞（SMC）的相互作用：< β >-VLDL （[^3H]胆固醇酯标记）与巨噬细胞孵育，并在平滑肌细胞中加入条件培养基。与不含巨噬细胞的培养液相比，在含有巨噬细胞的< β >-VLDL培养液中孵育后，SMC的放射性掺入量增加。在含有巨噬细胞的IDL培养基中也观察到SMC中放射性的增加。巨噬细胞调节< β >-VLDL或IDL产生脂质蛋白颗粒（d = 1.19, < β >-迁移率）。这些结果提示巨噬细胞- smc相互作用可能促进< β >-VLDL泡沫细胞的形成。或IDL.2。内皮细胞与平滑肌细胞的相互作用：从主动脉介质中培养内侧SMC，从血管内膜培养内膜SMC。内膜SMC增生明显高于内侧SMC。这些SMC与内皮细胞共培养后，内侧SMC的增殖受到抑制，内膜SMC的增殖受到抑制。提示SMC的增殖受内皮细胞的调控，内皮细胞的缺失可能促进内侧SMC的增殖。

1 Interaction between macrophages and smooth muscle cells (SMC):<beta>-VLDL ([^3H]cholesterol ester labeled ) was incubated with macrophages and the conditioned medium was added to the smooth muscle cells. The incorporated radioactivities into SMC were increased by incubation with <beta>-VLDL containing medium conditioned with macrophages, comparing to those conditioned without macrophages. The increase in incorporated radioactivities into SMC was also obseryed with IDL containing medium conditioned with macrophage. Conditioning of <beta>-VLDL or IDL with macrophages produced lipid-protein particles (d = 1.19, <beta>-mobility). These results suggest that macrophage-SMC interaction might promote the foam cell formation with <beta>-VLDL.or IDL.2. Interaction between endothelial cells and smooth muscle cells:Medial SMC was cultured from aortic media and intimal SMC was cultured from canulated aortic intima. The intiaml SMC proliferation increased comparing to that of medial SMC. By co-culturing of these SMC with endothelial cells, the proliferation of medial SMC was inhibited, but proliferation of intimal SMC was bit inhibited. These results suggest that SMC proliferation was regulated by endothelial cells, and loss of endothelial cell may promote proliferation of medial SMC.