Methods and Results: After rat aortic denudation injury the neointimal cell number increased several 100-fold between days 4 and 28, preceded by a 5-fold increase in the number of adventitial cells and a 4-fold increase in the number of adventitial microvessels. The influx, migration, and maturation of neointimal cells were quantitated by culturing whole vessel explants at different time points after injury. JSH-23 molecular weight Explant outgrowth increased 14-fold, and cell migration 3.5-fold on days 2-14 after injury. Cell proliferation increased less than 2-fold. The frequency of precursors to outgrowing cells, determined using

limiting dilution analysis, increased 8-fold between days 2 and 4 after injury. Many outgrowing cells displayed characteristics of undifferentiated cells. Conclusions: Adventitial activation precedes development of the neointima, and precursor cell influx occurs on days 2-14 after injury. Cell migration, more than proliferation, contributes to fibrointimal dysplasia. learn more These findings underline the importance of early therapeutic intervention with antimigratory compounds to prevent neointimal hyperplasia. Copyright (C) 2009 S. Karger AG, Basel”
“Angiogenesis is essential for the growth

and maturation of the ovarian follicle and its transition into the corpus luteum. In addition to the main proangiogenic factors, vascular endothelial growth factor (VEGF) and basic fibroblast

growth factor (bFGF), follicular fluid (FF) contains the hormone prolactin (PRL), which is known to promote angiogenesis in vivo. Here, we show that FF from large follicles, which contains twice the PRL level of FF from small follicles, stimulates endothelial cell proliferation to a greater extent than the latter, and that immunoneutralization of PRL prevents FF from stimulating endothelial cell proliferation. Notably, the FF increases the expression of the short and long PRL receptor isoforms in endothelial cells, and a purified PRL standard stimulates endothelial cell proliferation but Plasma membrane Ca2+ ATPase only after the cells have been pretreated with FF. However, purified PRL activates the JAK2/STAT3 pathway in endothelial cells in the absence of pretreatment with FF. In summary, PRL present in the FF stimulates the proliferation of endothelial cells. This effect likely involves the upregulation of the short and long PRL receptor isoforms and is independent of PRL-induced JAK2/STAT3 signaling. Copyright (C) 2009 S. Karger AG, Basel”
“Background: Atherosclerotic epicardial coronary arteries are a major cause of acute myocardial infarction (AMI). Recently, we found that intramyocardial capillaries may also play a role in AMI induction. We have now evaluated intramyocardial capillaries using ultrastructural analysis in AMI patients. Methods: 43 AMI patients (with AMI in the left ventricle) and 27 controls.