Publications by authors named "Isabella Baruscotti"
Article Synopsis
- Adenosine Inhibition
- : The study found that adenosine, specifically through the use of a stable analogue called 2-chloroadenosine, effectively reduces the migration and proliferation of c-Kit+ progenitor smooth muscle cells (P-SMCs), which are linked to neointimal thickening after injury.
- Mechanism of Action
- : 2-chloroadenosine works by increasing cyclic AMP levels, which in turn decreases the activation of pathways that promote cell growth (like cyclin D1) and increases the expression of regulators that slow down cell cycle progression (like p27).
- In Vivo Results
- : In tests on rats, treatment with 2-ch
Endothelial progenitor cells (EPCs) repair damaged endothelium and promote capillary formation, processes involving receptor tyrosine kinases (RTKs) and heme oxygenase 1 (HO-1). Because estradiol augments vascular repair, we hypothesize that estradiol increases EPC proliferation and capillary formation via RTK activation and induction of HO-1. Physiological concentrations of estradiol (10 nmol/L) increased EPC-induced capillary sprout and lumen formation in matrigel/fibrin/collagen systems.
View Article and Find Full Text PDFBackground: Endothelial progenitor cells play a pivotal role in tissue repair, and thus are used for cell replacement therapies in "regenerative medicine." We tested whether the anesthetic sevoflurane would modulate growth or mobilization of these angiogenic cells.
Methods: In an in vitro model, mononuclear cells isolated from peripheral blood of healthy donors were preconditioned with sevoflurane (3 times 30 min at 2 vol% interspersed by 30 min of air).