Expression of adhesion molecules and growth factors in vascular endothelial cell

内皮-白细胞粘附分子，如VCAM-1和ICAM-1，与循环单核细胞和t淋巴细胞募集到动脉粥样硬化病变有关。此外，平滑肌生长因子，包括PDGF A和B链以及HB-EGF，似乎在医学平滑肌细胞向动脉粥样硬化内膜的迁移和增殖中起着至关重要的作用。溶血磷脂酰胆碱（Ox-LDL）可转录诱导培养血管内皮细胞中VCAM-1、ICAM-1、PFGF和HB-EGF的表达；因此，我们试图确定lyso- pc诱导表达的转录和信号转导机制。我们发现细胞内环AMP水平升高可抑制lyso- pc诱导的PDGF和ICAM-1的表达。此外，lyso- pc诱导的PDGF表达依赖于蛋白酪氨酸磷酸化。因此，我们探索了能够在酪氨酸残基中快速磷酸化的蛋白质。我们发现一个分子质量为130kDa的蛋白，被命名为p130，被lyso-PC快速和短暂地酪氨酸磷酸化。通过免疫印迹和免疫沉淀，我们确定p130为PECAM-1，在培养的内皮细胞的细胞间连接处表达。我们的研究还表明，MAP激酶，如ERK和JNK，被lyso-PC激活，这似乎依赖于蛋白酪氨酸磷酸化。

Endothelial-leukocyte adhesion molecules such as VCAM-1 and ICAM-1, have been implicated in recruitment of circulating monocytes and T-lymphocytes to atherosclerotic lesions. In addition, smooth muscle growth factors, including PDGF A and B chains and HB-EGF, appear to play crucial role in migration and proliferation of medical smooth muscle cells into atherosclerotic intima. Lysophosphatidylcholine (Ox-LDL), can transcriptionally induce expression of VCAM-1, ICAM-1, PFGF, and HB-EGF in cultured vascular endothelial cells; therefore, we sought to define transcriptional and sibnal transduction mechanisms involved in lyso-PC-induced expression. We have found that elevated levels of intracelluar cyclic AMP inhibited lyso-PC-induced expression of PDGF and ICAM-1. Furthermore, lyso-PC-induced expression of PDGF was dependent upon protein tyrosine phosphorylation. We, therefore, explored the protein that can rapidly phosphorylated in the tyrosine residue. We revealed that a protein with a molecular mass of 130kDa, which was designated p130, was rapidly and transiently tyrosine phosphorylated by lyso-PC. By use of immunoblotting and immunoprecipitation, we have identified p130 as PECAM-1 which was expressed on the intercellular junction of cultured endothelial cells. Our study also have demonstrated that MAP kinases, such as ERK and JNK, were activated by lyso-PC, which appeared to depend upon protein tyrosine phosphorylation.