BMP‐2 and FGF‐2 Synergistically Facilitate Adoption of a Cardiac Phenotype in Somatic Bone Marrow c‐kit+/Sca‐1+ Stem Cells

DeGeorge, Brent R.; Rosenberg, Marc J.; Eckstein, Volker; Gao, Erhe; Herzog, Nicole; Katus, Hugo A.; Koch, Walter J.; Frey, Norbert; Most, Patrick

doi:10.1111/j.1752-8062.2008.00034.x

Cited by 22 publications

(13 citation statements)

References 45 publications

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“…We have used this new method to investigate the mechanism of MI and I/R injury by using both pharmacological tools 17, 18, 20-25 as well as genetic manipulation 5, 11, 26-33 . We have also used this quicker method involving a ‘heart pop-out’ procedure in stem cell 4 ; 34 and gene therapy studies (unpublished data), where we injected stem cells or adenovirus directly into the border zone of the ischemic heart while the heart was exposed. Our experience with this new and rapid method proves that it is extremely reproducible.…”

Section: Discussionmentioning

confidence: 99%

A Novel and Efficient Model of Coronary Artery Ligation and Myocardial Infarction in the Mouse

Gao

Lei

Shang

et al. 2010

Circulation Research

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Rationale: Coronary artery ligation to induce myocardial infarction (MI) in mice is typically performed by an invasive and time-consuming approach that requires ventilation and chest opening (classic method), often resulting in extensive tissue damage and high mortality. We developed a novel and rapid surgical method to induce MI that does not require ventilation.Objective: The purpose of this study was to develop and comprehensively describe this method and directly compare it to the classic method. Key Words: myocardial ischemia Ⅲ myocardial ischemia/reperfusion injury Ⅲ cardiac injury Ⅲ cardiac dysfunction Ⅲ mouse model C ardiovascular disease represents the leading cause of morbidity and death in developed countries. Coronary heart disease, which is the single largest cause of cardiovascular disease, is the narrowing of arteries over time caused by atherosclerotic plaques or the acute occlusion of the coronary artery by thrombosis, both of which lead to possible myocardial infarction (MI) and the eventual development of heart failure. 1,2 Protection from coronary heart disease-induced damage of the myocardium during myocardial ischemia/ reperfusion (I/R) injury has been a target of investigation for the development of innovative cardioprotective therapies. [3][4][5][6][7] The increase in the availability of various types of genetically manipulated mice has brought about the need for more efficient ways to induce myocardial damage for both molecular mechanistic studies and potentially therapeutic interventions. Two of the most common models used by researchers are permanent left main descending coronary artery (LCA) occlusion to induce a MI and also temporary coronary artery occlusion to induce I/R injury. 8,9 The I/R model is generally used to examine the short-term consequences of ischemic injury, whereas the MI model is usually used to investigate myocardial changes such as remodeling that occur over an extended period of time. Although a variety of surgical manipulations have been used during the past decade to induce the ischemic event, ligation of the LCA is still the most commonly practiced method. 3,9 -11 However, most investigators still use a method requiring ventilation and wide opening the chest (referred to as the classic method), which can cause extensive tissue damage, high surgical-related death and can also be quite time consuming for most surgeons. [12][13][14][15] Over the last few years, we have developed a new MI approach in mice that does not require ventilation. 11,16 -18 Complete characterization and description of this model has Original Methods and Results:

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Section: Discussionmentioning

confidence: 99%

A Novel and Efficient Model of Coronary Artery Ligation and Myocardial Infarction in the Mouse

Gao

Lei

Shang

et al. 2010

Circulation Research

Self Cite

587

462

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“…Engineered heart tissue from rat cardiomyocytes showed enhanced contractile performance at baseline and in response to βAR stimulation after S100A1 gene addition [74] indicating that S100A1-based genetic manipulation might be a promising strategy to strengthen therapeutic effectiveness of arteficial cardiac tissue or even artificial hearts. In addition, it is reasonable to assume that either bone-marrow or cardiac derived progenitor cells with the ability to regenerate cardiomyocytes [75, 76] could be subject to S100A1 gene addition prior to their therapeutic use. Such strategies could potentially result in newly formed cardiac cells with superior contractile properties and enhanced resistance against apoptosis, hypertrophic and proarrhythmic alterations.…”

Section: S100a1 In Cardiovascular Pathology and Therapeutic Potentialmentioning

confidence: 99%

S100A1 in cardiovascular health and disease: Closing the gap between basic science and clinical therapy

Kraus

Rohde

Weidenhammer

et al. 2009

Journal of Molecular and Cellular Cardiology

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Calcium (Ca 2+ ) signaling plays a major role in a wide range of physiological functions including control and regulation of cardiac and skeletal muscle performance and vascular tone [1,2]. As all Ca 2+ signals require proteins to relay intracellular Ca 2+ oscillations downstream to different signaling networks, a specific toolkit of Ca 2+ -sensor proteins involving members of the EF-hand S100 Ca 2+ binding protein superfamily maintains the integrity of the Ca 2+ signaling in a variety of cardiac and vascular cells, transmitting the message with great precision and in a temporally and spatially coordinated manner [3][4][5][6]. Indeed, the possibility that S100 proteins might contribute to heart and vascular diseases was first suggested by the discovery of distinctive patterns of S100 expression in healthy and diseased hearts and vasculature from humans and animal heart failure (HF) models [7][8][9][10][11][12][13][14][15][16][17][18]. Based on more elaborate genetic studies in mice and strategies to manipulate S100 protein expression in human cardiac, skeletal muscle and vascular cells, it is now apparent that the integrity of distinct S100 protein isoforms in striated muscle and vascular cells such as S100A1, S100A4, S100A6, S100A8/A9 or S100B is a basic requirement for normal cardiovascular and muscular development and function; loss of integrity would naturally lead to profound deregulation of the implicated Ca 2+ signaling systems with detrimental consequences to cardiac, skeletal muscle, and vascular function [7][8][9][10][11][12][13][14][15][16][17][18][19][20]. The brief debate and discussion here are confined by design to the biological actions and pathophysiological relevance of the EF-hand Ca 2+ -sensor protein S100A1 in the heart, vasculature and skeletal muscle with a particular focus on current translational therapeutic strategies [4,21,22]. By virtue of its ability to modulate the activity of numerous key effector proteins that are essentially involved in the control of Ca 2+ -and NO-homeostasis in cardiac, sketelal muscle and vascular cells, S100A1 has been proven to play a critical role both in cardiac performance, blood pressure regulation and skeletal muscle function [4,21,23]. Given that deregulated S100A1 expression in cardiomyocytes and endothelial cells has recently been linked to heart failure and Corresponding author: Patrick Most,

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“…These data suggested that both developing factors are essential for endothelial and cardiomyocyte differentiation. Although this concept has been described previously, in the work herein we have shown that the culture enrichment with ECs is able to upregulates these developing factors in vitro and enhance the differentiation of ESCs toward different cell lineages [22][23][24][25]. BMP-2 inhibition by NOG reduced expression of NF-L without affecting nestin expression.…”

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confidence: 80%

Bone Morphogenetic Protein-2/-4 Upregulation Promoted by Endothelial Cells in Coculture Enhances Mouse Embryoid Body Differentiation

Talavera-Adame

Gupta²,

Kurtovic³

et al. 2013

Stem Cells and Development

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Endothelial cells (ECs) provide inductive signals for cell differentiation in vivo. However, it is unknown if these cells promote such differentiation in vitro and the signals involved. We investigated whether ECs are able to enhance the differentiation of the three germ layers and the underlying mechanisms. We established a coculture system of mouse embryoid bodies (EBs) and ECs. Then, we analyzed the expression of markers representative of the three germ layers, such as PDX-1, proinsulin, insulin1 (endoderm), nestin, neurofilament light (ectoderm), CD31, cardiotin, and cardiac troponin I (mesoderm) in EBs cultured alone (controls) or with ECs. A significant increase of these markers was observed in EBs cocultured with ECs compared to controls. The cocultured EBs also exhibited more robust vascular networks similar to those EBs treated with bone morphogenetic protein-2 or -4 (BMP-2 or -4). Therefore, the role of these peptides in the differentiation was investigated. We found a significant upregulation of BMP-2/-4 and BMP receptor 1A in EBs treated with EC conditioned medium (EC-CM) at early or middle stages of EB development. Recombinant human BMP-2 and BMP-4 exerted similar effects than EC-CM in the expression of BMPs or in the upregulation of the three germ layer specific markers. BMP-2/-4 antagonists, such as noggin and chordinlike-1, respectively inhibited the EC-CM inductive effects. These results demonstrate that ECs enhance the differentiation in vitro of cells that derived from the three germ layers and that BMP-2/-4 play a central role in this process.

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BMP‐2 and FGF‐2 Synergistically Facilitate Adoption of a Cardiac Phenotype in Somatic Bone Marrow c‐kit+/Sca‐1+ Stem Cells

Cited by 22 publications

References 45 publications

A Novel and Efficient Model of Coronary Artery Ligation and Myocardial Infarction in the Mouse

A Novel and Efficient Model of Coronary Artery Ligation and Myocardial Infarction in the Mouse

S100A1 in cardiovascular health and disease: Closing the gap between basic science and clinical therapy

Bone Morphogenetic Protein-2/-4 Upregulation Promoted by Endothelial Cells in Coculture Enhances Mouse Embryoid Body Differentiation

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