Essential role of endothelial intric oxide synthase for mobilization os stem and progenitor cells
Article Abstract:
Research shows that impairment in neovascularization is caused by lack of endothelial nitric oxide synthase, which is in turn related to defect in progenitor cell mobilization from the bone marrow. Furthermore, under endothelial nitric oxide synthase deficient conditions, stem cell mobilizing metalloproteinase-9 is reduced in the bone marrow leading to impairment of stem cells as well.
Publication Name: Nature Medicine
Subject: Health
ISSN: 1078-8956
Year: 2003
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Low nitric oxide bioavailability contributes to the genesis of experimental cerebral malaria
Article Abstract:
Studies were conducted to determine whether an increase in nitric oxide (NO) bioavailability in the vasculature contributes to the genesis of experimental cerebral malaria (ECM). The results suggest that restoring NO bioavailability might represent an important component of effective adjunct therapy to rescue individuals from severe falciparum malaria.
Publication Name: Nature Medicine
Subject: Health
ISSN: 1078-8956
Year: 2006
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Cathepsin L is required for endothelial progenitor cell-induced neovascularization
Article Abstract:
The protease cathepsin L (CathL) was highly expressed in endothelial progenitor cells (EPC) as opposed to endothelial cells and was essential for matrix degradation and invasion by EPC in vitro. CathL has a critical role in the integration of circulating EPC into ischemic tissue and is required for EPC-mediated neovascularization.
Publication Name: Nature Medicine
Subject: Health
ISSN: 1078-8956
Year: 2005
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