Stem cell-derived cardiomyocytes after bone marrow and heart transplantation

Weger, Roel A. de; Verbrugge, Inge; Bruggink, Annette H.; Oosterhout, M M van; Souza, Yves De; Wichen, D.F. van; Gmelig-Meyling, F.H.J.; Jonge, Nicolaas de; Verdonck, Leo F.

doi:10.1038/sj.bmt.1705939

Cited by 16 publications

(12 citation statements)

References 33 publications

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“…Over the last decade, the dogma that the heart is a post-mitotic organ has been successfully challenged with growing evidence that cardiomyocytes undergo chimerism [37–39]. The mechanisms responsible for cardiomyocyte chimerism are poorly understood.…”

Section: Sphingolipids In Chronic Ischemic Heart Diseasementioning

confidence: 99%

Lysophospholipids in coronary artery and chronic ischemic heart disease

Abdel‐Latif

Heron

Morris

et al. 2015

Current Opinion in Lipidology

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Purpose of review The bioactive lysophospholipids, lysophosphatidic acid (LPA) and sphingosine 1 phosphate (S1P) have potent effects on blood and vascular cells. This review focuses their potential contributions to the development of atherosclerosis, acute complications, such as acute myocardial infarction, and chronic ischemic cardiac damage. Recent findings Exciting recent developments have provided insight into the molecular underpinnings of LPA and S1P receptor signaling. New lines of evidence suggest roles for these pathways in the development of atherosclerosis. In experimental animal models, the production, signaling and metabolism of LPA may be influenced by environmental factors in the diet that synergize to promote the progression of atherosclerotic vascular disease. This is supported by observations of human polymorphisms in the lysophospholipid metabolizing enzyme, PPAP2B, that are associated with risk of coronary artery disease and myocardial infarction. S1P signaling protects from myocardial damage that follows acute and chronic ischemia both by direct effects on cardiomyocytes and through stem cell recruitment to ischemic tissue. Summary This review will suggest novel strategies to prevent the complications of coronary artery disease by targeting LPA production and signaling. Additionally, ways in which S1P signaling pathways may be harnessed to attenuate ischemia-induced cardiac dysfunction will be explored.

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Section: Sphingolipids In Chronic Ischemic Heart Diseasementioning

confidence: 99%

Lysophospholipids in coronary artery and chronic ischemic heart disease

Abdel‐Latif

Heron

Morris

et al. 2015

Current Opinion in Lipidology

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“…Acute myocardial infarction (MI) initiates a cascade of events that result in mobilization of stem/primitive cell subpopulations from the bone marrow into the peripheral blood (PB) following the gradient of chemoattractant cytokines such as SDF-1α, LIF and HGF [6-11]. Furthermore, there is a growing line of evidence that cardiomyocytes undergo continuous renewal, maintained at least in part by BM-derived stem cells (BMSCs) [12-15], accounting for up to 45% of their total number by the age of 75 [16]. Because of their known contribution to cardiomyocyte renewal and the ease with which they can be isolated and subsequently delivered, BM-derived stem cells (BMSCs) represent an attractive cell population for myocardial regenerative therapies.…”

Section: Introductionmentioning

confidence: 99%

Evidence of mobilization of pluripotent stem cells into peripheral blood of patients with myocardial ischemia

Abdel‐Latif

Zuba‐Surma

Ziada

et al. 2010

Experimental Hematology

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Objective-The ischemic myocardium releases multiple chemotactic factors responsible for the mobilization and recruitment of bone marrow-derived cells to injured myocardium. However, the mobilization of primitive pluripotent stem cells (PSCs) enriched in Very Small Embryonic-Like stem cells (VSELs) in various cardiac ischemic scenarios is not well understood.Methods-Fifty four ischemic heart disease patients, including subjects with stable angina, non-ST elevation (NSTME) myocardial infarction (MI) and ST elevation myocardial infarction (STEMI), and twelve matched controls were enrolled. The absolute numbers of circulating stem/ primitive cells in samples of peripheral blood (PB) were quantitated by Image Stream Analysis and conventional flow cytometry. Gene expression of PSC (Oct-4 and Nanog), early cardiomyocyte (Nkx-2.5 and GATA-4), and endothelial (vWF) markers was analyzed by real-time PCR.Results-The absolute numbers of PSCs, stem cell populations enriched in VSELs and hematopoietic stem cells (HSCs) present in PB were significantly higher in STEMI patients at presentation and declined over time. There was a corresponding increase in pluripotent, cardiac and endothelial gene expression in unfractionated PB cells and sorted PB-derived primitive CD34+ cells. The absolute numbers of circulating VSELs and HSCs in STEMI correlated negatively with patients' age. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Conclusions-MyocardialConflict of interest disclosure: None. STEMI, which may represent a therapeutic window for future clinical applications. Reduced stem cell mobilization with advancing age could explain, in part, the observation that age is associated with poor prognosis in patients with MI. NIH Public Access

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“…While the mechanisms of cardiomyocyte renewal are poorly understood, this process is capable of renewing up to half of the cardiomyocytes during the normal life span [12]. In rodents, this phenomenon is dynamic, responds to myocardial injury [13], and is maintained, at least in part, by BM-derived cells [14]. AMI initiates innate reparatory mechanisms through which non-HSCs are mobilized from BM into peripheral blood (PB) and chemoattracted to the ischemic myocardium, a process that can potentially contribute to myocardial regeneration as we and others have demonstrated [15][16][17][18][19][20].…”

Section: Introductionmentioning

confidence: 99%

Bioactive Lipids and Cationic Antimicrobial Peptides as New Potential Regulators for Trafficking of Bone Marrow-Derived Stem Cells in Patients with Acute Myocardial Infarction

Karapetyan

Klyachkin

Selim

et al. 2013

Stem Cells and Development

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Acute myocardial infarction (AMI) triggers mobilization of stem cells from bone marrow (BM) into peripheral blood (PB). Based on our observation that the bioactive sphingophospholipids, sphingosine-1 phosphate (S1P), and ceramide-1 phosphate (C1P) regulate trafficking of hematopoietic stem cells (HSCs), we explored whether they also direct trafficking of non-hematopoietic stem cells (non-HSCs). We detected a 3-6-fold increase in circulating CD34 + , CD133 + , and CXCR4 + lineage-negative (Lin -)/CD45 -cells that are enriched in nonHSCs [including endothelial progenitors (EPCs) and very small embryonic-like stem cells (VSELs)] in PB from AMI patients (P < 0.05 vs. controls). Concurrently, we measured a *3-fold increase in S1P and C1P levels in plasma from AMI patients. At the same time, plasma obtained at hospital admission and 6 h after AMI strongly chemoattracted human BM-derived CD34 + /Lin -and CXCR4 + /Lin -cells in Transwell chemotaxis assays. This effect of plasma was blunted after depletion of S1P level by charcoal stripping and was further inhibited by the specific S1P1 receptor antagonist such as W146 and VPC23019. We also noted that the expression of S1P receptor 1 (S1P1), which is dominant in naïve BM, is reduced after the exposure to S1P at concentrations similar to the plasma S1P levels in patients with AMI, thus influencing the role of S1P in homing to the injured myocardium. Therefore, we examined mechanisms, other than bioactive lipids, that may contribute to the homing of BM non-HSCs to the infarcted myocardium. Hypoxic cardiac tissue increases the expression of cathelicidin and b-2 defensin, which could explain why PB cells isolated from patients with AMI migrated more efficiently to a low, yet physiological, gradient of stromal-derived factor-1 in Transwell migration assays. Together, these observations suggest that while elevated S1P and C1P levels early in the course of AMI may trigger mobilization of non-HSCs into PB, cathelicidin and b-2 defensin could play an important role in their homing to damaged myocardium.

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Stem cell-derived cardiomyocytes after bone marrow and heart transplantation

Cited by 16 publications

References 33 publications

Lysophospholipids in coronary artery and chronic ischemic heart disease

Lysophospholipids in coronary artery and chronic ischemic heart disease

Evidence of mobilization of pluripotent stem cells into peripheral blood of patients with myocardial ischemia

Bioactive Lipids and Cationic Antimicrobial Peptides as New Potential Regulators for Trafficking of Bone Marrow-Derived Stem Cells in Patients with Acute Myocardial Infarction

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