Immigration of Inflammatory Cells

Gap junctions are aggregates of intercellular channels, formed by head-to-head alignment of two he-michaimels (connections), each of which is made up of six coimexin protein molecules (Harold et al. 1997). Zhang etal. (1999) demonstrated that hypoxia-reoxygenation induced a temporal reduction of gap junctional intercellular communication in human umbihcal vein endothelial cells and that the protein tyrosine kinase pathway was primarily responsible for this gap junctional intercellular communication abnormality. 

Prostacyclin (PGI2) synthesised by endothelial cells and released predominantly towards the luminal side (Bassenge and Heusch 1990), acts via a receptor-mediated adenylate cyclase. In platelets, the increase in cAMP inhibits adhesion, aggregation and the release of pro-aggregatory and vasoconstrictor compounds such as serotonin, thromboxane A2, and ADR 

On stimulation, endothelial cells express membrane glycoproteins, that recognize Ugands on polymorphonuclear leucocytes (Carlos and Harlan 1990, Geng etal. 1990, Patel etal. 1991, Pigott et al. 1992, Franzini et al. 1995). This phenomenon is responsible for increased polymorphonuclear leucocyte penetration into myocardial tissue and also sustains inflammation. 

From oxidant-stimulated (2xl0 M hypoxan-thine/4.5 mil xanthine oxidase for 15 min) human umbilical vein endothelial cells cultured in vitro, Franzini etal. (1995) concluded that cAMP is probably involved in the adherence of polymorphonuclear neutrophils. Preincubation with pentoxifylline inhibited adherence in a concentration-dependent manner. Isobutylmethylxanthine and isopren-aline, which increase intracellular cAMP content, were also inhibitory. 

It is still unclear whether neutrophil binding to the endothelial cell surface affects VE-cadherin functions (Vestweber 2000). It was proposed that adhesion of polymorphonuclear leucocytes to human umbilical endothelial cells leads to the disorganisation of the VE-cadherin-dependent endothe- 

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Cytokinetic investigations revealed the appearance of a G2 block and the immigration of inflammatory cells belonging to the host defensive system after in vivo application of titanocene or vanadocene dichloride. After treatment in vitro, cell arrests at the Gi/ S boundary and in G2 were induced. These results correspond to the findings observed after administration of other cytostatic agents interfering with the nucleic add metabolism. 

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