Cellular response in preventing or inducing atherosclerosis

1. 我们研究了p21^<Sdi/Cip/Waf1> (p21)，一种由层流剪切应力（LS）诱导的生长抑制剂，在单核细胞粘附内皮细胞（ECs）中的作用。p21过表达抑制了扰动剪切应力（DS）诱导的EC增殖和单核细胞粘附。p21过表达显著抑制ds诱导的硫氧还蛋白相互作用蛋白、血管细胞粘附分子和趋化因子的表达，提示p21可能通过调节氧化还原平衡起到防止动脉粥样硬化的作用，从而抑制LS下ECs粘附分子的表达。2. 牙龈卟啉单胞菌（Pg）蛋白（Pg- r40kda）主要存在于72-82%的人主动脉粥样硬化的巨噬细胞中，而不存在于脂肪条纹、DIT和冠状动脉粥样硬化中。经Pg- lps刺激的巨噬细胞条件培养基诱导内皮细胞中TLR2 mRNA的表达，表明Pg诱导动脉粥样硬化，调节内皮细胞与巨噬细胞之间的炎症串扰

1. We examined the role of p21^<Sdi/Cip/Waf1> (p21), a growth inhibitor induced by laminar shear stress (LS), in monocyte adhesion to endothelial cells (ECs). Both EC proliferation and monocyte adhesion induced by disturbed shear stress (DS) were inhibited by p21-overexpression. p21-overexpression significantly suppressed the DS-induced expression of thioredoxin interacting protein, vascular cell adhesion molecule and chemokines, indicating that p21 may function to prevent atherogenesis by regulating the redox balance, which leads to the inhibition of adhesion molecule expression in ECs under LS. 2. Porphyromonas gingivalis (Pg) protein (Pg-r40kDa) was detected mainly in macrophages in 72-82% of human aortic atheromas, but not Fatty streak, DIT and coronary atheromas. Conditioned medium from macrophages stimulated with Pg-LPS induced the expression of TLR2 mRNA in ECs, indicating that Pg induces atherosclerosis, regulating the inflammatory cross talk between ECs and macrophages