Figures & data
Figure 1. CD133‐positive endothelial progenitor cells (EPC) characterized by the lack of CD34 represent a functionally active subpopulation of cells which are upregulated during ischemia (upper panel) and which have a significant better reendothelialization potential compared to CD133+/CD34+ EPC. Adapted from Friedrich et al. Citation18.
Figure 2. EPC were assessed in sham‐operated (Sham), ovariectomized (Ovarex), and ovariectomized mice with concomitant estrogen replacement treatment (Ovarex+E) by flow cytometry analysis to quantify Sca‐1/VEGF‐R2 positive EPC. A: Quantitative analysis of circulating numbers of Sca1 and VEGF‐R2 positive cells in peripheral blood (mean±SEM, n = 8, *P<0.05). B: Quantitative analysis of Sca1/VEGF‐R2 positive cells in the bone marrow (mean±SEM, n = 8, *P<0.05). Adapted from Strehlow et al. Citation31. (EPC = endothelial progenitor cells; Sca‐1 = stem cell antigen‐1; VEGF‐R2 = vascular endothelial growth factor receptor‐2.)
Figure 3. Endogenous stem cell mobilization requires the active recruitment of stromal cell‐bound stem cells mediated by proteases to the vascularized zones of the bone marrow. Stem cells then interact with the bone marrow endothelial cells to mobilize activated stem and progenitor cells to the peripheral blood. Various agents have been shown to effectively influence stem cell mobilization. (5‐FU = 5‐fluorouracil; CXCR‐4 = chemokine (CXC motif) receptor‐4; eNOS = endothelial nitric oxide synthase; FGF‐2 = fibroblast growth factor‐2; G‐CSF = granulocyte colony‐stimulating factor; GM‐CSF = granulocyte‐macrophage colony stimulating factor; ICAM‐1 = intercellular adhesion molecule‐1; LFA‐1 = leukocyte functional antigen‐1; mAb = monoclonal antibody; mKitL = membranous kit ligand; MMP‐9 = matrix metalloproteinase‐9; NO = nitric oxide; PlGF = placenta growth factor; SCF = stem cell factor; SDF‐1 = stromal derived factor‐1; sKitL = soluble kit ligand; VCAM‐1 = vascular cell adhesion molecule‐1; VEGF = vascular endothelial growth factor; VLA‐4 = very late antigen‐4.)
Figure 4. Circulating endothelial progenitor cells are predictive for the occurrence of a first major cardiovascular event in patients with coronary artery disease. The risk for the combined end point is reduced in a step‐wise fashion with increasing endothelial progenitor cell (EPC) levels. Adapted from Werner et al. Citation42.
Figure 5. Endothelial cell apoptosis is associated with the release of small membrane vesicles, the so‐called endothelial microparticles (EMP). Microparticle size ranges from 0.1–1.5 µm and derive from platelets, monocytes, erythrocytes, granulocytes, lymphocytes or endothelial cells. They express antigens derived from their mother cell and the negatively charged phosphatidylserine, which is normally exclusively located in the inner, cytoplasmic membrane but becomes surface‐exposed after cell activation or apoptosis. EMP can be quantified in peripheral blood by annexin V binding in combination with an endothelial cell marker, e.g. CD31 or vascular endothelial (VE)‐cadherin. P = 0.002 severe versus control P = <0.005. Modified from Sabatier et al. and Preston et al. Citation3,4. * acute coronary syndrome.
Figure 6. EPC contribute to the rejuvenation of the endothelial monolayer after endothelial cell damage. The effective regeneration of the endothelial monolayer might be a prerequisite for the prevention of atherosclerotic lesion formation. Cardiovascular risk factors negatively influence EPC number and function while the vast majority of cardioprotective agents mediate their action at least in part by positively influencing EPC. The pool of EPC consists of a heterogeneous population of cells which may interact in concert in the mediation of endothelial healing.(EPC = endothelial progenitor cells; G‐CSF = granulocyte colony‐stimulating factor; MNC = mononuclear cells; SCF = stem cell factor; VEGF = vascular endothelial growth factor.)
