Direct cardiac injection of G-CSF mobilized bone-marrow stem-cells improves ventricular function in old myocardial infarction

Archundia, Abel; Aceves, José Luis; López-Hernández, Manuel; Alvarado, Martha; Rodríguez, Enrique; Quiroz, Guillermo Díaz; Páez, Araceli; Rojas, Felipe Massó; Montaño, Luis F.

doi:10.1016/j.lfs.2005.04.080

Cited by 50 publications

(28 citation statements)

References 32 publications

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“…3 In addition, purified human CD34 ϩ progenitor cells are known to improve cardiac function in mice 30 and in patients after myocardial infarction. 31,32 It is noteworthy that the highly proangiogenic cell population of EPCs coexpressing markers such as CD133 and flk1 can be isolated from CD34 ϩ hematopoietic progenitors. 4 The potential of hematopoietic cells to transdifferentiate into myocardial cells is controversial, because there are reports describing their transdifferentiation into cardiomyocytes 5,6 and reports that challenge this potential.…”

Section: Org Frommentioning

confidence: 99%

The angiogenic factor CCN1 promotes adhesion and migration of circulating CD34+ progenitor cells: potential role in angiogenesis and endothelial regeneration

Grote¹,

Salguero²,

Ballmaier³

et al. 2007

Blood

105

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IntroductionBone marrow-derived and circulating hematopoietic progenitor cells have been shown to contribute to cardiovascular tissue regeneration. 1,2 CD34 ϩ hematopoietic progenitor cells were widely and successfully used in different transplantation models, including myocardial regeneration. 3 A subset of circulating CD34 ϩ cellsexpressing markers such as CD133 and vascular endothelial growth factor (VEGF) receptor-2 (flk1)-are endothelial progenitor cells (EPCs) with the ability to differentiate into mature endothelial cells, thus contributing to re-endothelialization and neovascularization. 4 In contrast, the ability of hematopoietic cells to transdifferentiate into functional cardiomyocytes is controversial. [5][6][7][8] Moreover, enhanced angiogenesis in response to progenitor cells may be influenced mainly by the release of growth factors rather than by cellular differentiation. 9 CCN1 (formerly known as CYR61) is a cysteine-rich heparinbinding protein that is encoded by an immediate early gene and belongs to the novel CCN gene family (connective tissue growth factor [CTGF], cysteine-rich angiogenic protein 61 [CYR61], and nephroblastoma overexpressed [Nov]). 10 The expression of CCN1 is rapidly induced in response to growth factors. 11 CCN1 is expressed by all types of vascular cells, is associated with the extracellular matrix (ECM) and mediates cell adhesion, migration, proliferation and neovascularization through cell type-specific binding mainly to ␣ 6 ␤ 1 , ␣ M ␤ 2 , and ␣ V ␤ 3 integrins. 10,[12][13][14] It is noteworthy that CCN1-deficient mice suffer embryonic death as a result of placental vascular insufficiency and compromised vessel integrity because of impaired vessel bifurcations and impaired VEGF-C expression, establishing CCN1 as a novel and essential regulator of vascular development. 15 In addition, it has been shown recently that CCN1 is critically involved in cardiac development. 16 Besides its ability to promote tumor growth, 17 we recently reported that enhanced CCN1 expression is associated with several cardiovascular pathophysiologic settings, such as atherosclerotic plaque formation, 18 enhanced vascular mechanical stretch, 19 cardiac pressure overload, and ischemic cardiomyopathy. 20 Recent evidence suggested that CCN1 expression is induced in various cardiovascular disorders, suggesting a role for CCN1 in cellular and tissue self-renewal, potentially involving circulating progenitor cells. Because the impact of CCN1 on progenitor cells is largely unknown, we used circulating human bone marrow-derived CD34 ϩ cells to study CCN1 effects on migration, release of growth factors, endothelial proliferation and neovascularization, which are important for cardiovascular regeneration. Materials and methods ReagentsAll chemicals were obtained from Sigma (Taufkirchen, Germany) unless otherwise specified. All cell culture plates were from TTP (Trasadingen, Switzerland). RGD peptides (Arg-Gly-Asp) and GRGDSP peptides (GlyArg-Gly-Asp-Ser-Pro) were from Bachem (Weil am Rhein, Germany). Human ...

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Section: Org Frommentioning

confidence: 99%

The angiogenic factor CCN1 promotes adhesion and migration of circulating CD34+ progenitor cells: potential role in angiogenesis and endothelial regeneration

Grote¹,

Salguero²,

Ballmaier³

et al. 2007

Blood

105

View full text Add to dashboard Cite

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“…In all 3 studies, the patients were treated with G-CSF followed by apheresis and selection of CD34+ cells. One study involved 5 patient with old MI (Archundia et al 2005), the second involved 20 patient with AMI (Steinwender et al 2006). …”

Section: Cell Therapy For Angiogenesis For Cadmentioning

confidence: 99%

Therapeutic myocardial angiogenesis

Renault

Losordo

2007

Microvascular Research

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“…Early clinical trials have demonstrated that G-CSF treatments show beneficial effects to improve cardiac function and myocardial perfusion in patients with acute myocardial infarction (AMI) [9][10][11][12][13] and chronic ischemic heart disease 14,15) . Although three subsequent double-blind placebo-controlled trials showed that G-CSF therapy failed to improve left ventricular restoration in AMI patients 16) , recent metaanalysis suggested that G-CSF may potentially benefit AMI patients with impaired left ventricular ejection fraction at baseline and when therapy is initiated early 17) .…”

Section: Introductionmentioning

confidence: 99%

Appropriate doses of Granulocyte-Colony Stimulating Factor Reduced Atherosclerotic Plaque Formation and Increased Plaque Stability in Cholesterol-Fed Rabbits

Matsumoto

Watanabe

Ueno

et al. 2010

JAT

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Aim:To evaluate the dose-response effects of granulocyte-colony stimulating factor (G-CSF) on atherosclerosis, we examined how G-CSF treatment at different concentrations affects atherosclerotic plaque formation in the aorta of cholesterol-fed rabbits. Methods: Japanese White rabbits (n 8 each) fed on a 1.5% cholesterol diet were subcutaneously injected with G-CSF at 50 (GL), 100 (GM), or 300 g/kg/day (GH) for five days, or with 3 cycles of G-CSF at 100 g/kg/day at 3-week intervals (GM3), or human serum albumin (Control). The extent and composition of atherosclerosis was evaluated 14 weeks after cholesterol feeding. Results: Although G-CSF treatment did not affect plasma lipid levels, the percentage of aortic surface involvement in the GM3 group was significantly decreased (p 0.05) compared with the Control group. Histological analysis revealed that the intima media ratio was also diminished in GM and GM3 groups. The extent of intimal smooth muscle cell accumulation was higher in GL and GM3 groups than in the Control group. TIMP-2 mRNA expression in the aortic tissue was increased by G-CSF treatment. Conclusions: Our results suggest that appropriate doses of G-CSF reduced atherosclerotic plaque formation and increased plaque stability in cholesterol-fed rabbits.J Atheroscler Thromb, 2010; 17:84-96.

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Direct cardiac injection of G-CSF mobilized bone-marrow stem-cells improves ventricular function in old myocardial infarction

Cited by 50 publications

References 32 publications

The angiogenic factor CCN1 promotes adhesion and migration of circulating CD34+ progenitor cells: potential role in angiogenesis and endothelial regeneration

The angiogenic factor CCN1 promotes adhesion and migration of circulating CD34+ progenitor cells: potential role in angiogenesis and endothelial regeneration

Therapeutic myocardial angiogenesis

Appropriate doses of Granulocyte-Colony Stimulating Factor Reduced Atherosclerotic Plaque Formation and Increased Plaque Stability in Cholesterol-Fed Rabbits

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