Essential role of endothelial nitric oxide synthase for mobilization of stem and progenitor cells
By Alexandra Aicher, C. Heeschen, Christiane Mildner-Rihm, C. Urbich, C. Ihling, K. Technau‐Ihling, A. Zeiher, Stefanie Dimmeler. Nature Medicine, 2003
1,426 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/613f520ecd474914b216f206f74893f1064e4f0b
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Citations in the corpus
- Nitric oxide synthases: regulation and function. (2012, background): “Reduced systemic NO bioactivity seen in ischaemic heart disease may therefore contribute to impaired neovascularization.(92)”
- Endothelial Dysfunction and Diabetes: Effects on Angiogenesis, Vascular Remodeling, and Wound Healing (2012, background): “These alterations in NO signaling might contribute to modulation of postischemic neovascularization because NO is a well-known mediator of BM-MNC mobilization and differentiation, as well as basal neovascularization reaction [85].”
- Endothelial dysfunction. (2004, background): “It is interesting that eNOS expression by bone marrow stroma cells plays an essential role in the recruitment of endothelial progenitor cells (145).”
- The Role of MicroRNAs in Human Diseases (2010, background): “Recently it was demonstrated that eNOS also plays a major role in the mobilization and functional activity of stem cells (68 - 70) ; therefore, designing miRNAs to target eNOS is thought to regulate vasculogenesis (62) .”
- The role of nitric oxide in tumour progression (2006, background): “showed that defects in angiogenesis and reperfusion in ischaemic tissues of eNos −/− mice could be rescued by injection of stem/progenitor cells that were derived from wild-type mic”
- Pleiotropic effects of statins. (2005, result): “These findings agree with earlier data showing that statins rapidly mobilize EPCs from the bone marrow and accelerate vascular structure formation via activation of phosphatidylinositol 3kinase (PI3K)/protein kinase Akt and eNOS (55,74,76).”
- The SDF-1-CXCR4 signaling pathway: a molecular hub modulating neo-angiogenesis. (2007, background): “Remarkably, activation of MMP-9 and subsequent release of sKitL and mobilization of pro-angiogenic cells are impaired in eNOS−/− mice, delineating a new role for the NO signaling pathway in SDF-1-induced BM cell mobilization [37].”
- Vascular complications of diabetes: mechanisms of injury and protective factors (2013, background): “Differentiation of EPC from bone-marrow-derived cells may also play a role (Tamarat et al., 2004). eNOS is necessary for mobilization of EPC from the bone marrow, as this phenomenon is impaired in eNOS knockout mice (Aicher et al., 2003).”
- Cytokines in atherosclerosis: pathogenic and regulatory pathways. (2006, background): “eNOS is a potent proangiogenic mediator (5), previously shown to limit atherosclerosis development (346).”