Importance of recruitment of bone marrow-derived CXCR4+ cells in post-infarct cardiac repair mediated by G-CSF

Yu, Ming; Takemura, Genzou; Arai, M.; Ohno, Takamasa; Onogi, Hirohito; Takahashi, Tomoyuki; Minatoguchi, Shinya; Fujiwara, Takako; Fujiwara, Hisayoshi

doi:10.1016/j.cardiores.2006.05.002

Cited by 69 publications

(68 citation statements)

References 28 publications

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“…G-CSF is also efficient in inducing the mobilization of angiogenic BM cells, including CD34 + CD133 + VEGFR2 + EPCs, in addition to directly promoting angiogenesis, in part by upregulating SDF-1 [75][76][77]. The promising efficacy of G-CSF in supporting organ regeneration in animal studies is currently being tested in clinical trials [78].…”

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

527

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: 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

527

382

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“…SDF-1 released from a myoblast sheet could mobilize CXCR4+ cells to the injured myocardium [2]. Moreover, stem-cell mobilization and homing therapy by G-CSF was introduced to another myocardial regeneration treatment as an alternative to cellular cardiomyoplasty [73,74].…”

Section: Paracrine Effect Of Cytokines After Cellular Cardiomyoplastymentioning

confidence: 99%

From bench to bedside, work in cell-based myocardial regeneration therapy

Miyagawa

Sawa²

2014

JBiSE

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In clinical cellular cardiomyoplasty, bone marrow cells and myoblasts are introduced mainly to ischemic cardiomyopathy tissue via several cell delivery systems, such as needle injection or catheter. These clinical studies have demonstrated the safety and feasibility of this technique, but its effectiveness for treating heart failure, especially in the long term, is still under discussion. Neither of these cell types can differentiate into cardiomyocytes; rather, they improve the failing heart mainly by the paracrine effects of some cytokines, such as Hepatocyte growth factor (HGF) and Vascular endothelial growth factor (VEGF). Thus, many researchers have a great interest in stem cells, which exist in bone marrow, circulating blood, atrium, and adipose tissue, and can differentiate into cardiomyocytes. Although several stem cells with the potential to differentiate into various cell types have been reported, few can differentiate into cardiomyocytes. Moreover, beating cells that can demonstrate synchronized contraction with native cardiomyocytes are critical for the complete repair of severe heart failure. Therefore, stem cells with a high differentiation capacity should be explored for the goal of completely repairing severely damaged myocardium. In this review, we summarize the clinical protocols and basic experiments for cellular cardiomyoplasty using bone marrow cells, myoblasts, and other stem cells.

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“…These authors reported that even though c-kit + increased from 0.05 to 2.8% in peripheral blood, growth factor treated mice did not improve their cardiac function performance, or decreased MI size or any sign of cardiac regeneration as well as cell therapy. Until that time, the mechanism of G-CSF action was discussed exclusively by increasing cell mobilization and homing to ischemic heart with conflicting results [6,8,[10][11][12][13].…”

Section: Pre-clinical Experimentsmentioning

confidence: 99%