Regular ArticleHypoxia Stimulates Human Endothelial Cells to Release Smooth Muscle Cell Mitogens: Role of Prostaglandins and bFGF
References (0)
Cited by (77)
Bone Marrow Mesenchymal Stem Cells in Organ Repair and Strategies to Optimize their Efficacy
2011, Regenerative NephrologyFibroblast growth factor-2 transiently activates the p53 oncosuppressor protein in human primary vascular smooth muscle cells: Implications for atherogenesis
2010, AtherosclerosisCitation Excerpt :During their life-time, humans can be continuously exposed to atherogenic factors [49]. As all those factors can recruit FGF-2-producing cells in the blood vessel walls [3,5–9,14,15,37,50], VSMC are likely to be repeatedly (chronically) exposed to FGF-2. Upon any contact, FGF-2 could then bi-modally, time-dependently modulate the activity and/or expression of p53 or its targets.
Time-dependent phenotypic and contractile changes of pulmonary artery in chronic hypoxia-induced pulmonary hypertension
2009, Journal of Pharmacological SciencesRegional changes in the masseter muscle of rats after reduction of blood supply
2007, Annals of AnatomyDiscordant effects of nicotine on endothelial cell proliferation, migration, and the inward rectifier potassium current
2005, Journal of Molecular and Cellular CardiologyCitation Excerpt :Vascular endothelial cells play an essential role in the process of angiogenesis and vessel repair. Basic fibroblast growth factor (bFGF), which is released from endothelial cells and macrophages during hypoxia or vascular injury, takes part in this process by influencing endothelial proliferation and migration [1–4]. Nicotine is a major component of cigarette smoke.
Influence of ischemic injury on vein graft remodeling: Role of cyclic adenosine monophosphate second messenger pathway in enhanced vein graft preservation
2005, Journal of Thoracic and Cardiovascular Surgery