Overexpression of Stromal Cell–derived Factor-1 Enhances Endothelium-supported Transmigration, Maintenance, and Proliferation of Hematopoietic Progenitor Cells

Hwang, Jin-Hee; Kim, Seong-Woo; Park, Sang-Eun; Yun, Hwan‐Jung; Lee, Younghee; Kim, Samyong; Jo, Deog‐Yeon

doi:10.1089/scd.2006.15.260

Cited by 16 publications

(9 citation statements)

References 32 publications

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“…SDF-1 is key in recruitment of monocytes/macrophages and their perivascular retention around new blood vessels that arise from neovascularlization 12 . SDF-1 mediates proliferation, adhesion, migration, and homing of circulating progenitor cells that express the SDF-1 receptor CXCR4 and monocytes, thereby promoting tissue regeneration 4, 18, 49 . Further, SDF-1 causes proliferation of CD34+ cells and differentiation of these cells into macrophages and foam cells 48 .…”

Section: Discussionmentioning

confidence: 99%

Stromal cell–derived factor-1 promoted angiogenesis and inflammatory cell infiltration in aneurysm walls

Hoh¹,

Hosaka

Downes

et al. 2014

JNS

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Object A small percentage of cerebral aneurysms rupture, but when they do, the effects are devastating. Current management of unruptured aneurysms consist of surgery, endovascular treatment, or watchful waiting. If the biology of how aneurysms grow and rupture were better known, a novel drug could be developed to prevent unruptured aneurysms from rupturing. Ruptured cerebral aneurysms are characterized by inflammation-mediated wall remodeling. We studied the role of stromal cell-derived factor-1 (SDF-1) in inflammation-mediated wall remodeling in cerebral aneurysms. Methods Human aneurysms; murine carotid aneurysms; and murine intracranial aneurysms were studied by immunohistochemistry. Flow cytometry analysis was performed on blood from mice developing carotid aneurysms or intracranial aneurysms. The effect of SDF-1 on endothelial cells and macrophages was studied by chemotaxis cell migration assay and capillary tube formation assay. Anti-SDF-1 blocking antibody was given to mice and compared to control (vehicle)-administered mice for its effects on the walls of carotid aneurysms and the development of intracranial aneurysms. Results Human aneurysms, murine carotid aneurysms, and murine intracranial aneurysms, all express SDF-1; and mice with developing carotid aneurysms or intracranial aneurysms have increased progenitor cells expressing CXCR4, the receptor for SDF-1 (P<0.01 and P<0.001, respectively). Human aneurysms and murine carotid aneurysms have endothelial cells, macrophages, and capillaries in the walls of the aneurysms; and the presence of capillaries in the walls of human aneurysms is associated with presence of macrophages (P=0.01). SDF-1 promotes endothelial cell and macrophage migration (P<0.01 for each), and promotes capillary tube formation (P<0.001). When mice are given anti-SDF-1 blocking antibody, there is a significant reduction in endothelial cells (P<0.05), capillaries (P<0.05), and cell proliferation (P<0.05) in the aneurysm wall. Mice given anti-SDF-1 blocking antibody develop significantly fewer intracranial aneurysms (33% versus 89% in mice given control IgG)(P<0.05). Conclusions These data suggest SDF-1 associated with angiogenesis and inflammatory cell migration and proliferation in the walls of aneurysms, and may have a role in the development of intracranial aneurysms.

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Section: Discussionmentioning

confidence: 99%

Stromal cell–derived factor-1 promoted angiogenesis and inflammatory cell infiltration in aneurysm walls

Hoh¹,

Hosaka

Downes

et al. 2014

JNS

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“…[7][8][9]16,24 Enhanced SDF-1 expression and production in the endothelium is essential for the engraftment of human stem cells and for their maintenance in situ. 7,8,20,25 Ex vivo exposure of EPCs to SDF-1 before their injection would be expected to enhance their recruitment from the circulation to ischemic tissue and, thus, their graft efficiency.…”

Section: Discussionmentioning

confidence: 99%

Ex Vivo Priming of Endothelial Progenitor Cells With SDF-1 Before Transplantation Could Increase Their Proangiogenic Potential

Zemani

Silvestre

Fauvel-Lafève

et al. 2008

ATVB

170

153

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Objectives-As SDF-1 and its cognate receptor CXCR4 play a key role in the survival and mobilization of immature cells, we examined whether preconditioning of endothelial progenitor cells (EPCs) with SDF-1 could further promote their capacity to enhance angiogenesis. Methods and Results-EPC exposure to 100 ng/mL SDF-1 for 30 min induced a proangiogenic phenotype, with cell migration and differentiation into vascular cords in Matrigel and increased their therapeutic potential in a nude mouse model of hindlimb ischemia. This pretreatment enhanced EPC adhesion to activated endothelium in physiological conditions of blood flow by stimulating integrin-mediated EPCs binding to endothelial cells. Pretreated EPCs showed significantly upregulated surface ␣4 and ␣M integrin subunit expression involved in the homing of immature cells to a neovasculature and enhanced FGF-2 and promatrix metalloproteinase (MMP)-2 secretion. All these effects were significantly attenuated by EPC incubation with AMD-3100, a CXCR4 antagonist, by prior HSPGs disruption and by HUVEC incubation with anti-intercellular adhesion molecule1 (ICAM-1) and anti-vascular cell adhesion molecule (VCAM) blocking antibodies. Pretreated EPCs adhered very rapidly (within minutes) and were resistant to shear stresses of up to 2500s Ϫ1 . Key Words: endothelial progenitor cells Ⅲ SDF-1 Ⅲ ischemia Ⅲ HSPGs Ⅲ adhesion T he discovery of bone marrow-derived endothelial progenitor cells (EPCs) in peripheral blood prompted an intensive search for new ways of inducing neovascularization in patients with heart and limb ischemia, based on transplantation of bone marrow-or peripheral blood-derived EPCs. 1,2 Several studies indicated that local implantation of ex vivoexpanded EPCs improved neovascularization of damaged tissues in animal models of hindlimb ischemia. [2][3][4][5] Contrary to differentiated endothelial cells, administration of EPCs led to increased blood flow in ischemic limbs of nude mice. These immature cells promote neovascularization by differentiating in situ into endothelial cells and by secreting growth factors, cytokines, and proteases that support angiogenic and vasculogenic processes. 6 -8 However, transplantation of autologous EPCs has several limitations, including the limited supply of expanded progenitors, the time required to harvest, expand, and reinject autologous EPCs, and poor graft efficiency. In addition, EPCs appear to undergo unfavorable functional changes during the expansion procedure. 9 This may explain why the capacity of injected EPCs to promote neovascularization is highly variable and depends on the experimental model. 1,10 The yield is currently so low that very large blood volumes would have to be processed to obtain sufficient EPCs for therapeutic use. The required number of EPCs can be reduced by using local infusion 3,5,11 or by concomitant infusion of proangiogenic proteins. 4,12 In addition, EPCs can be activated before their injection 3,5,10 or mobilized into the circulation by cytokines. 7,13 Cytokines released by damaged ti...

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“…As expected, normal human synovium (n ϭ 11) showed minimal VEGF-A staining ( Figure 1D). Because mobilization of EPCs and proangiogenic HPCs from the BM requires activation of MMPs, particularly MMP-9, and because SDF-1␣ has been shown to potently promote the migration and activation of mononuclear cells, including HPCs, 25,26 we stained HJD and control synovium for these mediators. We observed that MMP-9 ( Figure 1B) and SDF-1␣ ( Figure 1C), were highly expressed in the vascular endothelium, with moderate expression in synovial cells in the lining and sublining regions of the hemophilic synovium (n ϭ 12).…”

Section: Hjd Synovium Expresses Proangiogenic Mediators and Myeloid Cmentioning

confidence: 99%

Neoangiogenesis contributes to the development of hemophilic synovitis

Acharya

Kaplan

MacDonald

et al. 2011

Blood

110

121

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Joint arthropathy secondary to recurrent hemarthroses remains a debilitating complication of hemophilia despite the use of prophylactic factor concentrates. Increased vascularity and neoangiogenesis have been implicated in the progression of musculoskeletal disorders and tumor growth. We hypothesized that de novo blood vessel formation could play a major role in the pathogenesis of hemophilic joint disease (HJD). We observed a 4-fold elevation in proangiogenic factors (vascular endothelial growth factor-A [VEGF-A], stromal cell-derived factor-1, and matrix metalloprotease-9) and proangiogenic macrophage/monocyte cells (VEGF ؉ /CD68 ؉ and VEGFR1 ؉ /CD11b ؉ ) in the synovium and peripheral blood of HJD subjects along with significantly increased numbers of VEGFR2 ؉ /AC133 ؉ endothelial progenitor cells and CD34 ؉ / VEGFR1 ؉ hematopoietic progenitor cells. Sera from HJD subjects induced an angiogenic response in endothelial cells that was abrogated by blocking VEGF, whereas peripheral blood mononuclear cells from HJD subjects stimulated synovial cell proliferation, which was blocked by a human-

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Overexpression of Stromal Cell–derived Factor-1 Enhances Endothelium-supported Transmigration, Maintenance, and Proliferation of Hematopoietic Progenitor Cells

Cited by 16 publications

References 32 publications

Stromal cell–derived factor-1 promoted angiogenesis and inflammatory cell infiltration in aneurysm walls

Stromal cell–derived factor-1 promoted angiogenesis and inflammatory cell infiltration in aneurysm walls

Ex Vivo Priming of Endothelial Progenitor Cells With SDF-1 Before Transplantation Could Increase Their Proangiogenic Potential

Neoangiogenesis contributes to the development of hemophilic synovitis

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