ABSTRACT
OBJECTIVE: Placental growth factor (PIGF) mediates angiogenesis and inflammation, and is up-regulated in early and advanced atherosclerotic lesions. But its effects on the function of vascular endothelial cells is still largely unknown. This study was designed to test the effects of PIGF on the secretion of proinflammatory cytochemokines in vascular endothelial cells. METHODS: Cultured human umibilical vein endotheial cells (HUVECs) of passages 3-5 were used. Growth-arrested HUVECs were treated with 5, 10, 25 or 50 ng/mL recombinant human PIGF (rhPLGF) for 4, 8, 24 or 48 hours. Monocyte chemotactic protein-1 (MCP-1), soluble vascular cell adhesion molecule-1 (sVCAM-1) and P-selectin secreted from HUVECs were measured by ELISA. RESULTS: Treated with rhPIGF at 10-50 ng/mL for 48 h, the production of MCP-1 from the HUVECs increased significantly. Treatment with rhPIGF at 5-50 ng/mL for 4 h, the release of P-selectin from the HUVECs increased significantly. But rhPIGF (5-50 ng/mL) had no effect on sVCAM secretion. CONCLUSION: Exogenous PIGF could modulate the secretion function of vascular. endothelial cells, stimulating MCP-1 and P-selectin release in HUVECs.
Subject(s)
Cytokines/metabolism , Endothelial Cells/metabolism , Pregnancy Proteins/pharmacology , Umbilical Veins/cytology , Cells, Cultured , Chemokine CCL2/genetics , Chemokine CCL2/metabolism , Cytokines/biosynthesis , Cytokines/genetics , Endothelial Cells/cytology , Humans , P-Selectin/biosynthesis , P-Selectin/genetics , Placenta Growth Factor , Vascular Cell Adhesion Molecule-1/genetics , Vascular Cell Adhesion Molecule-1/metabolismABSTRACT
OBJECTIVE: To analyse the clinical factors that contribute to the rise of the cardiac injury marker troponin after coronary intervention and the impact of the rise of troponin on the clinical outcomes. METHODS: Troponin I was measured after elective coronary intervention in 129 patients whose baseline levels of troponin were normal. The clinical outcomes of the patients were follow-up. RESULTS: The rise of troponin I was associated with side branch losses, flow impairments such as no flow or slow flow and diabetes. The incidence of myocardial infarction increased with the rise of troponin I. The angina onsets were more common and the length of stay were longer in the patients with the rise of troponin I than those without. CONCLUSION: The rise of troponin after coronary intervention is related to the complex coronary lesions and the complications of intervention procedures. To a certain extent, the level of troponin can predict the patients' outcomes.
