Angiogenic cells can be rapidly mobilized and efficiently harvested from the blood following treatment with AMD3100

Shepherd, Rebecca; Capoccia, Benjamin J.; Devine, Steven M.; DiPersio, John F.; Trinkaus, Kathryn; Ingram, David A.; Link, Daniel C.

doi:10.1182/blood-2006-06-030577

Cited by 107 publications

(91 citation statements)

References 42 publications

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“…AMD3100 mobilizes human endothelial progenitor cells and proangiogenic cells into the peripheral blood in both the human and mice, although, in the murine studies, both endothelial and stromal progenitor cell mobilization was enhanced by VEGF pretreatment [16,17]. Interestingly, in the humans, more immature human endothelial progenitor cells or high proliferative potentialendothelial colony forming cells (HPP-ECFCs) are mobilized by AMD3100 than those with a lower proliferative potential [16]. Additionally, AMD3100 treatment can reduce blood vessel and tumor formation in preclinical models [18].…”

Section: Introductionmentioning

confidence: 95%

The Hematopoietic Chemokine CXCL12 Promotes Integration of Human Endothelial Colony Forming Cell–Derived Cells into Immature Vessel Networks

Newey

Tsaknakis

Khoo

et al. 2014

Stem Cells and Development

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Section: Introductionmentioning

confidence: 95%

The Hematopoietic Chemokine CXCL12 Promotes Integration of Human Endothelial Colony Forming Cell–Derived Cells into Immature Vessel Networks

Newey

Tsaknakis

Khoo

et al. 2014

Stem Cells and Development

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“…This apparent paradox emanates from the finding that a single injection of the CXCR4 antagonist, AMD3100, efficiently induces rapid mobilization of HSCs, pro-angiogenic cells and EPCs into the circulation [44,45] (Figure 2c). However, plasma elevation of SDF-1 also supports mobilization of BM cells over a period of several days, entertaining the notion that the mechanism by which CXCR4 inhibition or activation promotes mobilization is driven by two different molecular or cellular pathways.…”

Section: Paradox Of the Sdf-1-cxcr4 Signaling Pathway In The Regulatimentioning

confidence: 99%

The SDF-1–CXCR4 signaling pathway: a molecular hub modulating neo-angiogenesis

Petit

Jin

Rafii

2007

Trends in Immunology

528

382

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Pro-angiogenic bone marrow (BM) cells include subsets of hematopoietic cells that provide vascular support and endothelial progenitor cells (EPCs), which under certain permissive conditions could differentiate into functional vascular cells. Recent evidence demonstrates that the chemokine stromal-cell derived factor-1 (SDF-1, also known as CXCL12) has a major role in the recruitment and retention of CXCR4 + BM cells to the neo-angiogenic niches supporting revascularization of ischemic tissue and tumor growth. However, the precise mechanism by which activation of CXCR4 modulates neo-angiogenesis is not clear. SDF-1 not only promotes revascularization by engaging with CXCR4 expressed on the vascular cells but also supports mobilization of pro-angiogenic CXCR4 + VEGFR1 + hematopoietic cells, thereby accelerating revascularization of ischemic organs. Here, we attempt to define the multiple functions of the SDF-1-CXCR4 signaling pathway in the regulation of neo-vascularization during acute ischemia and tumor growth. In particular, we introduce the concept that, by modulating plasma SDF-1 levels, the CXCR4 antagonist AMD3100 acutely promotes, while chronic AMD3100 treatment inhibits, mobilization of pro-angiogenic cells. We will also discuss strategies to modulate the mobilization of essential subsets of BM cells that participate in neo-angiogenesis, setting up the stage for enhancing revascularization or targeting tumor vessels by exploiting CXCR4 agonists and antagonists, respectively.

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“…AMD3100 is a potent and rapid mobilizer of angiogenic cells [47], which may stimulate angiogenesis at sites of ischemia through a paracrine mechanism [48], including ischemia in a diabetic environment [49].…”

Section: Page 8 Of 30mentioning

confidence: 99%