Chylomicron remnants induce monocyte chemoattractant protein-1 expression via p38 MAPK activation in vascular smooth muscle cells

摘要: Chylomicron remnants, major lipoproteins at postprandial hyperlipidemia, have been considered to be proatherogenic lipoproteins. However, the mechanisms by which chylomicron remnants enhance atherosclerosis not fully understood. Monocyte chemoattractant protein-1 (MCP-1) is a chemokine stimulates migration of monocytes and plays critical role in development atherosclerosis. In this study, we investigated effect on MCP-1 expression cultured vascular smooth muscle cells (VSMCs). We prepared chylomicrons from lymph gastrostomized rats fed with egg solution obtained plasma hepatectomized were injected chylomicrons. Treatment VSMC resulted significant increase mRNA protein time-and dose-dependent manner. Further, activated p38 mitogen-activated kinase (MAPK) extracellular signal-regulated (ERK1/2). Pretreatment VSMCs MAPK inhibitors, SB203580 SB202190, inhibition remnants-induced expression, whereas inhibitor, PD98059, had no these responses. secretion was much more pronounced than those chylomicrons, oxidized low-density lipoproteins, or lysophosphatidylcholine. These results indicated that stimulated VSMCs, suggested might contribute formation through proinflammatory effect.