A Relationship Between Vascular Endothelial Growth Factor, Angiogenesis, and Cardiac Repair After Muscle Stem Cell Transplantation Into Ischemic Hearts

Payne, Thomas R.; Oshima, Hideki; Okada, Minoru; Momoi, Nobuo; Tobita, Kimimasa; Keller, Bradley B.; Peng, Hairong; Huard, Johnny

doi:10.1016/j.jacc.2007.04.100

Cited by 134 publications

(145 citation statements)

References 30 publications

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“…Several approaches to increase the number of CMs within injured myocardium have been attempted, including (1) activation and stimulation of host myocardial regeneration by transplanted cells via angiogenic and=or paracrine effects, 4,5 (2) direct transplantation of functional CMs or myogenic cells, [6][7][8] and (3) implantation of tissue constructs containing CMs. 9,10 In the latter two cases, the ideal donor CMs possess a high potential for division during cell preparation and potential for further proliferation following implantation to form a viable myocardial tissue within the surrounding injured recipient myocardium.…”

Section: Introductionmentioning

confidence: 99%

Engineered Early Embryonic Cardiac Tissue Increases Cardiomyocyte Proliferation by Cyclic Mechanical Stretch via p38-MAP Kinase Phosphorylation

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Tinney

Liu

et al. 2009

Tissue Engineering Part A

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Cardiomyocyte (CM) transplantation is one therapeutic option for cardiac repair. Studies suggest that fetal CMs display the best cell type for cardiac repair, which can finitely proliferate, integrate with injured host myocardium, and restore cardiac function. We have recently developed an engineered early embryonic cardiac tissue (EEECT) using embryonic cardiac cells and have shown that EEECT contractile properties and cellular proliferative response to cyclic mechanical stretch stimulation mimic developing fetal myocardium. However, it remains unknown whether cyclic mechanical stretch-mediated high cellular proliferation activity within EEECT reflects CM or non-CM population. Studies have shown that p38-mitogen-activated protein kinase (p38MAPK) plays an important role in both cyclic mechanical stretch stimulation and cellular proliferation. Therefore, in the present study, we tested the hypothesis that cyclic mechanical stretch (0.5 Hz, 5% strain for 48 h) specifically increases EEECT CM proliferation mediated by p38MAPK activity. Cyclic mechanical stretch increased CM, but not non-CM, proliferation and increased p38MAPK phosphorylation. Treatment of EEECT with the p38MAPK inhibitor, SB202190, reduced CM proliferation. The negative CM proliferation effects of SB202190 were not reversed by concurrent stretch stimulation. Results suggest that immature CM proliferation within EEECT can be positively regulated by mechanical stretch and negatively regulated by p38MAPK inhibition.

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Section: Introductionmentioning

confidence: 99%

Engineered Early Embryonic Cardiac Tissue Increases Cardiomyocyte Proliferation by Cyclic Mechanical Stretch via p38-MAP Kinase Phosphorylation

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Tinney

Liu

et al. 2009

Tissue Engineering Part A

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“…For example, improved cardiac repair after myocardial infarction has been shown to occur when vascular endothelial growth factor (VEGF) secretion is increased. 18 The activation of signaling pathways by pharmacologically preconditioning skeletal myoblasts promotes their survival by 1 inducing the release of paracrine factors that stimulate angiogenesis in the infarcted heart. 19 Mechanical and structural cues have been shown to play a critical role in tissue physiology, including cell growth, migration, gene expression, and cell signaling, 20,21 and this may play a role in cell transplantation since most cells and tissues experience biomechanical forces within the body.…”

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confidence: 99%

Mechanical Loading of Stem Cells for Improvement of Transplantation Outcome in a Model of Acute Myocardial Infarction: The Role of Loading History

Cassino

Drowley

Okada

et al. 2012

Tissue Engineering Part A

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Stem cell therapy for tissue repair is a rapidly evolving field and the factors that dictate the physiological responsiveness of stem cells remain under intense investigation. In this study we hypothesized that the mechanical loading history of muscle-derived stem cells (MDSCs) would significantly impact MDSC survival, host tissue angiogenesis, and myocardial function after MDSC transplantation into acutely infarcted myocardium. Mice with acute myocardial infarction by permanent left coronary artery ligation were injected with either nonstimulated (NS) or mechanically stimulated (MS) MDSCs. Mechanical stimulation consisted of stretching the cells with equibiaxial stretch with a magnitude of 10% and frequency of 0.5 Hz. MS cell-transplanted hearts showed improved cardiac contractility, increased numbers of host CD31 + cells, and decreased fibrosis, in the peri-infarct region, compared to the hearts treated with NS MDSCs. MS MDSCs displayed higher vascular endothelial growth factor expression than NS cells in vitro. These findings highlight an important role for cyclic mechanical loading preconditioning of donor MDSCs in optimizing MDSC transplantation for myocardial repair.

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“…Meanwhile, improved multipotency would account for regeneration of injured skeletal muscle tissue by possibly differentiating into multiple cell types including myofibers, blood vessel-related cells (smooth muscle cells and endothelial cells), and neurons. 12,19 At the molecular signaling level, Notch signaling functions either to maintain stemness or to initiate differentiation of multiple cell lineages, and ensures proper balance between stem cells and cells with a committed fate. 49,50 Notch signaling is also essential for myogenic development and the regenerative potential of skeletal muscle.…”

Section: Discussionmentioning

confidence: 99%

“…SASCs including MDSCs from noninjured muscles were able to release vascular endothelial growth factor and to induce angiogenesis in vivo. 12 In addition, muscle stem cells can differentiate into the endothelial cell lineage. 16 It seems that SASCs from injured muscle may contribute to angiogenesis by both directly differentiating into endothelial cells and creating a favorable environment for angiogenesis by releasing vascular endothelial growth factor.…”

Section: Sascs From Injured Muscle Repair Dystrophic Muscle More Effimentioning

confidence: 99%

“…Using MDSCs for tissue engineering application and cell transplantation into animals and patients has verified that these cells are highly efficient for stem cellbased therapies in various tissues including regeneration and repair of skeletal and cardiac muscle, bone, articular cartilage, and peripheral nerve. 8,[11][12][13][14][15][16][17][18][19] However, previous studies have been limited to SASCs isolated from healthy noninjured skeletal muscle, and SASCs from injured muscle have not as yet been characterized.…”

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Slow-Adhering Stem Cells Derived from Injured Skeletal Muscle Have Improved Regenerative Capacity

Xiang

Rathbone

et al. 2011

The American Journal of Pathology

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A wide variety of myogenic cell sources have been used for repair of injured and diseased muscle including muscle stem cells, which can be isolated from skeletal muscle as a group of slow-adhering cells on a collagen-coated surface. The therapeutic use of muscle stem cells for improving muscle regeneration is promising; however, the effect of injury on their characteristics and engraftment potential has yet to be described. In the present study, slow-adhering stem cells (SASCs) from both laceration-injured and control noninjured skeletal muscles in mice were isolated and studied. Migration and proliferation rates, multidifferentiation potentials, and differences in gene expression in both groups of cells were compared in vitro. Results demonstrated that a larger population of SASCs could be isolated from injured muscle than from control noninjured muscle. In addition, SASCs derived from injured muscle demonstrated improved migration, a higher rate of proliferation and multidifferentiation, and increased expression of Notch1, STAT3, Msx1, and MMP2. Moreover, when transplanted into dystrophic muscle in MDX/SCID mice, SASCs from injured muscle generated greater engraftments with a higher capillary density than did SASCs from control noninjured muscle. These data suggest that traumatic injury may modify stem cell characteristics through trophic factors and improve the transplantation potential of SASCs in alleviating skeletal muscle injuries and diseases.

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A Relationship Between Vascular Endothelial Growth Factor, Angiogenesis, and Cardiac Repair After Muscle Stem Cell Transplantation Into Ischemic Hearts

Abstract: Our findings suggest that VEGF is essential for the induction of angiogenesis and functional improvements observed after MDSC transplantation for infarct repair.

Cited by 134 publications

References 30 publications

Engineered Early Embryonic Cardiac Tissue Increases Cardiomyocyte Proliferation by Cyclic Mechanical Stretch via p38-MAP Kinase Phosphorylation

Engineered Early Embryonic Cardiac Tissue Increases Cardiomyocyte Proliferation by Cyclic Mechanical Stretch via p38-MAP Kinase Phosphorylation

Mechanical Loading of Stem Cells for Improvement of Transplantation Outcome in a Model of Acute Myocardial Infarction: The Role of Loading History

Slow-Adhering Stem Cells Derived from Injured Skeletal Muscle Have Improved Regenerative Capacity

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