Navab M, Imes S S, Hama S Y, Hough G P, Ross L A, Bork R W, Valente A J, Berliner J A, Drinkwater D C, Laks H
Department of Medicine, University of California Los Angeles 90024-167917.
J Clin Invest. 1991 Dec;88(6):2039-46. doi: 10.1172/JCI115532.
Incubation of cocultures of human aortic endothelial (HAEC) and smooth muscle cells (HASMC) with LDL in the presence of 5-10% human serum resulted in a 7.2-fold induction of mRNA for monocyte chemotactic protein 1 (MCP-1), a 2.5-fold increase in the levels of MCP-1 protein in the coculture supernatants, and a 7.1-fold increase in the transmigration of monocytes into the subendothelial space of the cocultures. Monocyte migration was inhibited by 91% by antibody to MCP-1. Media collected from the cocultures that had been incubated with LDL induced target endothelial cells (EC) to bind monocyte but not neutrophil-like cells. Media collected from cocultures that had been incubated with LDL-induced monocyte migration into the subendothelial space of other cocultures that had not been exposed to LDL. In contrast, media from separate cultures of EC or smooth muscle cells (SMC) containing equal number of EC or SMC compared to coculture and incubated with the same LDL did not induce monocyte migration when incubated with the target cocultures. High density lipoprotein HDL, when presented to cocultures together with LDL, reduced the increased monocyte transmigration by 91%. Virtually all of the HDL-mediated inhibition was accounted for by the HDL2 subfraction. HDL3 was essentially without effect. Apolipoprotein AI was also ineffective in preventing monocyte transmigration while phosphatidylcholine liposomes were as effective as HDL2 suggesting that lipid components of HDL2 may have been responsible for its action. Preincubating LDL with beta-carotene or with alpha-tocopherol did not reduce monocyte migration. However, pretreatment of LDL with probucol or pretreatment of the cocultures with probucol, beta-carotene, or alpha-tocopherol before the addition of LDL prevented the LDL-induced monocyte transmigration. Addition of HDL or probucol to LDL after the exposure to cocultures did not prevent the modified LDL from inducing monocyte transmigration in fresh cocultures. We conclude that cocultures of human aortic cells can modify LDL even in the presence of serum, resulting in the induction of MCP-1, and that HDL and antioxidants prevent the LDL induced monocyte transmigration.
在5%-10%人血清存在的情况下,将人主动脉内皮细胞(HAEC)和平滑肌细胞(HASMC)的共培养物与低密度脂蛋白(LDL)一起孵育,导致单核细胞趋化蛋白1(MCP-1)的mRNA诱导增加7.2倍,共培养物上清液中MCP-1蛋白水平增加2.5倍,单核细胞向共培养物内皮下空间的迁移增加7.1倍。抗MCP-1抗体可使单核细胞迁移受到91%的抑制。从与LDL孵育过的共培养物中收集的培养基可诱导靶内皮细胞(EC)结合单核细胞,但不结合中性粒细胞样细胞。从与LDL孵育过的共培养物中收集的培养基可诱导单核细胞迁移到未暴露于LDL的其他共培养物的内皮下空间。相比之下,与共培养物中内皮细胞或平滑肌细胞(SMC)数量相等、并与相同LDL孵育的单独培养的内皮细胞或平滑肌细胞的培养基,在与靶共培养物孵育时不会诱导单核细胞迁移。当高密度脂蛋白(HDL)与LDL一起加入共培养物时,可使增加的单核细胞迁移减少91%。几乎所有HDL介导的抑制作用都由HDL2亚组分引起。HDL3基本无作用。载脂蛋白AI在防止单核细胞迁移方面也无效,而磷脂酰胆碱脂质体与HDL2一样有效,这表明HDL2的脂质成分可能是其发挥作用的原因。用β-胡萝卜素或α-生育酚预孵育LDL不会减少单核细胞迁移。然而,在加入LDL之前,用普罗布考预处理LDL或用普罗布考、β-胡萝卜素或α-生育酚预处理共培养物可防止LDL诱导的单核细胞迁移。在共培养物暴露于LDL后再加入HDL或普罗布考,并不能阻止修饰后的LDL在新鲜共培养物中诱导单核细胞迁移。我们得出结论,即使在有血清存在的情况下,人主动脉细胞的共培养物也可修饰LDL,导致MCP-1的诱导,并且HDL和抗氧化剂可防止LDL诱导的单核细胞迁移。