Small peptide analogs to stromal derived factor–1 enhance chemotactic migration of human and mouse hematopoietic cells

Zhong, Rui-kun; Law, Ping; Wong, Donald; Merzouk, Ahmed; Salari, Hassan; Ball, Edward D.

doi:10.1016/j.exphem.2004.01.011

Cited by 31 publications

(22 citation statements)

References 22 publications

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“…The rapid mobilization of the HSCs induced by the CXCR4 antagonist AMD3100 suggests that cells in close apposition of vascular cells were forced to enter the circulation, appearing in the peripheral blood within an hour of interfering with SDF-1 binding to CXCR4. By contrast, SDF-1 or its agonists [49], or G-CSF, which require activation of a cascade of events and, possibly, cycling of hematopoietic cells, need several days to allow for the recruitment of quiescent tethered HSCs from the BM, delaying the entry of the cells to the peripheral circulation (Figure 2a).…”

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

confidence: 99%

“…The promising efficacy of G-CSF in supporting organ regeneration in animal studies is currently being tested in clinical trials [78]. Alternatively, promoting SDF-1 signaling could also be achieved by fucoidan-mediated SDF-1 elevation [79], or direct activation of the CXCR4 pathway with SDF-1 agonists [49], with FTY720, a sphingosine-1-phosphate analog that activates CXCR4 signaling [80] or soluble molecules priming CXCR4 + cells such as complement C3a [81].…”

Section: Delivery Of Sdf-1 For Stem Cell Therapy and Organ Revascularmentioning

confidence: 99%

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

Petit

Jin

Rafii

2007

Trends in Immunology

530

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

confidence: 99%

Section: Delivery Of Sdf-1 For Stem Cell Therapy and Organ Revascularmentioning

confidence: 99%

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

Petit

Jin

Rafii

2007

Trends in Immunology

530

382

View full text Add to dashboard Cite

show abstract

“…Therefore, the promising efficacy of G-CSF in supporting organ regeneration in animal studies is currently being tested in clinical trials [150]. Alternatively, promotion of CXCL12 signaling is being induced by fucoidanmediated CXCL12 elevation [151], or small peptide analogs to CXCL12 activating the CXCR4 signaling pathway [152], or with FTY 720, a sphingosine-1-phosphate analog that activates CXCR4 [153] or soluble molecules priming CXCR4? cells such as C3a [154].…”

Section: Addressing Cxcr4/cxcl12 In Angiogenesis/cancermentioning

confidence: 99%

Platelet-derived chemokines: pathophysiology and therapeutic aspects

Flad

Brandt

2010

Cell. Mol. Life Sci.

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The identification of chemokines in blood platelets has strengthened our view of these cells as participants in immune host defense. Platelet chemokines representing prestored and rapidly releasable proteins may play a major role as first-line inflammatory mediators. This is evident from their capability to recruit early inflammatory cells such as neutrophil granulocytes and monocytes and even to exhibit direct antimicrobial activity. However, insight is growing that platelet chemokines may be also long-term regulators, e.g., by activating T lymphocytes, by modulating the formation of endothelium and even thrombocytopoiesis itself. This review deals with the individual and cooperative functionality of platelet chemokines, as well as their potential as a basis for therapeutic intervention in the pathology of inflammation, infection, allergy and tumors. Within this context, therapeutic strategies based on the use of antibodies, modified chemokines, chemokine-binding proteins and chemokine receptor antagonists as well as first clinical studies will be addressed.

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“…[5] A second strategy is to enhance the recruitment of endogenous stem cells into the lesion site for tissue regeneration. Several factors, such as hepatocyte growth factor (HGF) [6] and stromal cell-derived factor-1 (SDF-1) [7] have shown chemotaxic effects on stem cells. In this study, we used HGF as a model factor to attract bone marrow MSCs into an extracellular matrix (ECM)-like hydrogel in vitro.…”

mentioning

confidence: 99%

Recruitment of Endogenous Stem Cells for Tissue Repair

Zhao

Zhang

Prestwich

et al. 2008

Macromolecular Bioscience

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The traditional concept of stem cell therapy envisions the isolation of stem cells from patients, propagation and differentiation in vitro, and subsequent re-injection of autologous cells into the patient. There are many problems associated with this paradigm, particularly during the in vitro manipulation process and the delivery and local retention of re-injected cells. An alternative paradigm that could be easier, safer, and more efficient, would involve attracting endogenous stem cells and precursor cells to the defect site for new tissue regeneration. Hepatocyte growth factor (HGF), a pleiotropic cytokine of mesenchymal origin, exerts a strong chemoattractive effect on mesenchymal stem cells (MSCs) and neural stem cells (NSCs), and induces migration of MSCs in vitro. However, HGF undergoes rapid proteolysis in vivo, which results in a very short lifetime of the bioactive cytokine. To maintain the therapeutic level of HGF at the defect site necessary for endogenous stem cell recruitment, sustained, long-term, and localized delivery of HGF is required. Thiol-modified glycosaminoglycans hyaluronan (HA) and heparin (HP), combined with modified gelatin (Gtn), have been crosslinked with poly(ethylene glycol) diacrylate (PEGDA) to afford semisynthetic ECM-like (sECM) hydrogels that can both provide controlled growth factor release and permit cell infiltration and proliferation. Herein we compare the use of different sECM compositions for controlled release of HGF and concomitant recruitment of human bone marrow MSCs into the scaffold in vitro. [Figure: see text].

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Small peptide analogs to stromal derived factor–1 enhance chemotactic migration of human and mouse hematopoietic cells

Cited by 31 publications

References 22 publications

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

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

Platelet-derived chemokines: pathophysiology and therapeutic aspects

Recruitment of Endogenous Stem Cells for Tissue Repair

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