Endothelial progenitor cells are resident in the bone marrow blood sinusoids and circulate in the peripheral circulation. They mobilize from the bone marrow after vascular injury and home to the site of injury where they differentiate into endothelial cells. Activation and mobilization of endothelial progenitor cells from the bone marrow is induced via the production and release of endothelial progenitor cell-activating factors and includes speciifc growth factors and cytokines in response to peripheral tissue hypoxia such as after acute ischemic stroke or trauma. Endotheli-al progenitor cells migrate and home to speciifc sites following ischemic stroke via growth factor/cytokine gradients. Some growth factors are less stable under acidic conditions of tissue isch-emia, and synthetic analogues that are stable at low pH may provide a more effective therapeutic approach for inducing endothelial progenitor cell mobilization and promoting cerebral neovas-cularization following ischemic stroke.

转染VEGF165的内皮祖细胞移植恢复糖尿病ED大鼠的勃起功能

Objective:To investigate protective effects ofMallotus furetianus(M. furetianus)on functions of endothelial progenitor cells (EPCs) in atherosclerotic rats.Methods:Atherosclerosis was established by intraperitoneal injection of vitamin D3 combined with high fat diet for 9 weeks. Extracts ofM. furetianus were given to prevent damage of EPCs in dose of 0.081 g/kg and 0.026 g/kg. Rats were sacrificed, and then mononuclear cells were isolated from bone marrow to culture EPCs and test the functions of EPCs.Results:M. furetianus can improve the capacities of EPCs on proliferation, migration, adhesion, and tubule formation in doses of 0.081 g/kg; improve adhesion, and tubule formation in dose of 0.026 g/kg in atherosclerotic rats. Conclusion:M. furetianus can protect functions of EPCs in atherosclerotic rats.

Background: Ongoing low-grade inflammation and endothelial dysfunction persist in children with coronary lesions diagnosed with Kawasaki disease (KD). Statins, frequently used in the management of high cholesterol, have also shown to improve surrogate markers of infl ammation and endothelial dysfunction. This study was undertaken to investigate the effi cacy and safety of pravastatin in children with coronary artery aneurysms due to KD.
Methods: The study enrolled 14 healthy children and 13 male children, aged 2-10 years, with medium-to-giant coronary aneurysms for at least 12 months after the onset of KD. Pravastatin was given orally to the KD group at a dose of 5 mg/day for children under 5 and 10 mg/day for children older than 5 years. To determine the effects of pravastatin on endothelial function, high-frequency ultrasound was performed before the start of the study and 6 months after pravastatin therapy. The parameters measured were brachial artery flow-mediated dilation (FMD), non-flow mediated dilation (NMD), and carotid artery stiffness index (SI). High sensitive C-reactive protein (hs-CRP) levels, the circulating endothelial progenitor cells (EPCs) number, and serum lipid profiles were also determined at baseline and after 6 months of pravastatin treatment.
Results: Before treatment, the KD group had significantly decreased FMD (P<0.05) and increased SI and hs-CRP levels (P<0.05) compared with controls. After 6 months of pravastatin therapy, FMD improved significantly compared to the baseline KD group (3.16±6.49 to 10.05±7.74, P<0.05), but remained significantly less than that in the control group with no signifi cant changes in NMD and SI. There were signifi cant decreases in markers of inflammation after treatment. The hs-CRP levels decreased signifi cantly from 2.93±0.81 mmol/L to 2.14±0.82 mmol/L (P<0.05) and the serum apo-B and apo-B/apo-A1 ratio were also reduced (P<0.05) in the KD group. However, the circulating EPC number was not signifi cantly different between baseline and that following pravastatin treatment in the KD group and the control group (P>0.05). No signifi cant complications were noted with paravastatin therapy.
Conclusions: Pravastatin improves endothelial function and reduces low-grade chronic infl ammation in patients with coronary aneurysms due to KD. Children with coronary aneurysms due to KD may benefit from statin therapy.