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  1. Article ; Online: Healing a Heart Through Genetic Intervention.

    James, Jeanne / Robbins, Jeffrey

    Circulation research

    2016  Volume 118, Issue 6, Page(s) 920–922

    MeSH term(s) Aging/genetics ; Animals ; CRISPR-Cas Systems/genetics ; Gene Deletion ; Myocardium/metabolism
    Language English
    Publishing date 2016-03-18
    Publishing country United States
    Document type Comment ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.116.308468
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Anti-inflammatory mechanisms and therapeutic opportunities in myocardial infarct healing.

    Kempf, Tibor / Zarbock, Alexander / Vestweber, Dietmar / Wollert, Kai C

    Journal of molecular medicine (Berlin, Germany)

    2012  Volume 90, Issue 4, Page(s) 361–369

    Abstract: ... tissue degradation leading to infarct expansion and heart failure. Genetic ablation or blockade ... cell types involved in infarct healing. Some anti-inflammatory interventions are therefore deleterious ... of necrotic debris by neutrophils, monocytes, and macrophages is a critical component of infarct healing ...

    Abstract The wound healing response after myocardial infarction (MI) involves a cascade of molecular and cellular events that lead to a replacement of the necrotic area with a collagen-rich scar. Clearance of necrotic debris by neutrophils, monocytes, and macrophages is a critical component of infarct healing; however, tight control and timely repression of this inflammatory response is important to prevent excessive tissue degradation leading to infarct expansion and heart failure. Genetic ablation or blockade of anti-inflammatory pathways tends to be detrimental after MI, whereas genetic ablation of pro-inflammatory pathways tends to be beneficial. Accordingly, therapies enhancing endogenous anti-inflammatory pathways or blocking endogenous pro-inflammatory pathways have been found to improve wound healing and to reduce the risk of heart failure in rodent models of acute MI. Besides their scavenger function, inflammatory cells promote healing by stimulating angiogenesis and granulation tissue formation via paracrine factors. Moreover, signaling mediators that are active in inflammatory cells may be active also in non-inflammatory cell types involved in infarct healing. Some anti-inflammatory interventions are therefore deleterious. However, interventions that carefully adjust the balance between the essential and detrimental facets of inflammation may provide new therapeutic opportunities for patients with large MIs who continue to be at risk of developing heart failure, despite modern reperfusion and anti-remodeling strategies.
    MeSH term(s) Animals ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Heart/drug effects ; Humans ; Inflammation/drug therapy ; Inflammation/etiology ; Inflammation/immunology ; Myocardial Infarction/complications ; Myocardial Infarction/drug therapy ; Myocardial Infarction/immunology ; Myocardium/immunology ; Signal Transduction/drug effects ; Wound Healing/drug effects
    Chemical Substances Anti-Inflammatory Agents
    Language English
    Publishing date 2012-01-07
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1223802-8
    ISSN 1432-1440 ; 0946-2716
    ISSN (online) 1432-1440
    ISSN 0946-2716
    DOI 10.1007/s00109-011-0847-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Monocyte-directed RNAi targeting CCR2 improves infarct healing in atherosclerosis-prone mice.

    Majmudar, Maulik D / Keliher, Edmund J / Heidt, Timo / Leuschner, Florian / Truelove, Jessica / Sena, Brena F / Gorbatov, Rostic / Iwamoto, Yoshiko / Dutta, Partha / Wojtkiewicz, Gregory / Courties, Gabriel / Sebas, Matt / Borodovsky, Anna / Fitzgerald, Kevin / Nolte, Marc W / Dickneite, Gerhard / Chen, John W / Anderson, Daniel G / Swirski, Filip K /
    Weissleder, Ralph / Nahrendorf, Matthias

    Circulation

    2013  Volume 127, Issue 20, Page(s) 2038–2046

    Abstract: ... subset-targeted RNAi altered infarct inflammation and healing.: Methods and results: Flow cytometry ... left ventricular remodeling. Inflammatory pathways may present a therapeutic target to prevent post-MI heart ... in infarcted hearts of apoE(-/-) mice that were treated with nanoparticle-encapsulated siRNA. To follow ...

    Abstract Background: Exaggerated and prolonged inflammation after myocardial infarction (MI) accelerates left ventricular remodeling. Inflammatory pathways may present a therapeutic target to prevent post-MI heart failure. However, the appropriate magnitude and timing of interventions are largely unknown, in part because noninvasive monitoring tools are lacking. Here, we used nanoparticle-facilitated silencing of CCR2, the chemokine receptor that governs inflammatory Ly-6C(high) monocyte subset traffic, to reduce infarct inflammation in apolipoprotein E-deficient (apoE(-/-)) mice after MI. We used dual-target positron emission tomography/magnetic resonance imaging of transglutaminase factor XIII (FXIII) and myeloperoxidase (MPO) activity to monitor how monocyte subset-targeted RNAi altered infarct inflammation and healing.
    Methods and results: Flow cytometry, gene expression analysis, and histology revealed reduced monocyte numbers and enhanced resolution of inflammation in infarcted hearts of apoE(-/-) mice that were treated with nanoparticle-encapsulated siRNA. To follow extracellular matrix cross-linking noninvasively, we developed a fluorine-18-labeled positron emission tomography agent ((18)F-FXIII). Recruitment of MPO-rich inflammatory leukocytes was imaged with a molecular magnetic resonance imaging sensor of MPO activity (MPO-Gd). Positron emission tomography/magnetic resonance imaging detected anti-inflammatory effects of intravenous nanoparticle-facilitated siRNA therapy (75% decrease of MPO-Gd signal; P<0.05), whereas (18)F-FXIII positron emission tomography reflected unimpeded matrix cross-linking in the infarct. Silencing of CCR2 during the first week after MI improved ejection fraction on day 21 after MI from 29% to 35% (P<0.05).
    Conclusion: CCR2-targeted RNAi reduced recruitment of Ly-6C(high) monocytes, attenuated infarct inflammation, and curbed post-MI left ventricular remodeling.
    MeSH term(s) Amino Acid Sequence ; Animals ; Atherosclerosis/genetics ; Atherosclerosis/pathology ; Atherosclerosis/therapy ; Female ; Gene Targeting/methods ; Genetic Predisposition to Disease ; Genetic Therapy/methods ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Monocytes/metabolism ; Monocytes/pathology ; Myocardial Infarction/genetics ; Myocardial Infarction/pathology ; Myocardial Infarction/therapy ; RNA Interference/physiology ; Random Allocation ; Receptors, CCR2/antagonists & inhibitors ; Receptors, CCR2/genetics ; Receptors, CCR2/metabolism ; Wound Healing/genetics
    Chemical Substances Ccr2 protein, mouse ; Receptors, CCR2
    Language English
    Publishing date 2013-04-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.112.000116
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: c-kit dysfunction impairs myocardial healing after infarction.

    Cimini, Massimo / Fazel, Shafie / Zhuo, Sun / Xaymardan, Munira / Fujii, Hiroko / Weisel, Richard D / Li, Ren-Ke

    Circulation

    2007  Volume 116, Issue 11 Suppl, Page(s) I77–82

    Abstract: ... the infiltration of c-kit+ cells to the infarcted heart may potentiate this endogenous repair response, prevent ... for facilitating healing, leading to efficient cardiac repair after myocardial infarction (MI).: Methods and ... impacts the myofibroblast repair response in infarcted hearts. Interventions that increase ...

    Abstract Background: We hypothesized that c-kit receptor function in the bone marrow is important for facilitating healing, leading to efficient cardiac repair after myocardial infarction (MI).
    Methods and results: We used Kit(W)/Kit(W-v) c-kit mutant mice and their wild-type littermates to assess the importance of c-kit function in cardiac remodeling after coronary ligation. We found that mutant mice developed 1.6-fold greater ventricular dilation (P=0.008) attributable to a 1.3-fold greater infarct expansion by day 14 after MI (P=0.01). The number of proliferating smooth muscle alpha-actin expressing cells was 1.8-fold lower in mutant mice at day 3 (P<0.01), resulting in a 1.6 to 1.8-fold reduction in total regional nonvascular smooth muscle alpha-actin expressing cells by both microscopy and flow cytometry (P<0.001 for both). This decrease was accompanied by a 1.4-fold reduction in the number of CD31 expressing blood vessels (P<0.05). Prior transplantation of wild-type bone marrow cells into mutant mice rescued the efficient establishment of vessel-rich repair tissue by inducing a 1.5-fold increase in nonvascular smooth muscle alpha-actin expressing cells and CD31 expressing blood vessels (P<0.05 for both). The increased recruitment of cells into the infarct region in the chimeric mice was associated with reduced infarct expansion (P<0.03) compared to wild-type levels.
    Conclusions: Bone marrow c-kit function critically impacts the myofibroblast repair response in infarcted hearts. Interventions that increase the infiltration of c-kit+ cells to the infarcted heart may potentiate this endogenous repair response, prevent infarct expansion, and improve the recovery of cardiac function after MI.
    MeSH term(s) Animals ; Bone Marrow Transplantation/methods ; Female ; Mice ; Mice, Mutant Strains ; Myocardial Infarction/genetics ; Myocardial Infarction/pathology ; Myocardial Infarction/physiopathology ; Myocardium/pathology ; Proto-Oncogene Proteins c-kit/genetics ; Proto-Oncogene Proteins c-kit/physiology
    Chemical Substances Proto-Oncogene Proteins c-kit (EC 2.7.10.1)
    Language English
    Publishing date 2007-09-11
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.107.708107
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Selective homocysteine lowering gene transfer improves infarct healing, attenuates remodelling, and enhances diastolic function after myocardial infarction in mice.

    Muthuramu, Ilayaraja / Jacobs, Frank / Singh, Neha / Gordts, Stephanie C / De Geest, Bart

    PloS one

    2013  Volume 8, Issue 5, Page(s) e63710

    Abstract: ... homocysteine lowering enhanced infarct healing as indicated by a 21% (p<0.01) reduction of infarct length ... lowering gene transfer improves infarct healing, attenuates remodelling, and significantly enhances ... Background and aims: Homocysteine levels predict heart failure incidence in prospective ...

    Abstract Background and aims: Homocysteine levels predict heart failure incidence in prospective epidemiological studies and correlate with severity of heart failure in cross-sectional surveys. The objective of this study was to evaluate whether a selective homocysteine lowering intervention beneficially affects cardiac remodelling and cardiac function after myocardial infarction (MI) in a murine model of combined hypercholesterolemia and hyperhomocysteinemia.
    Methodology and principal findings: A selective homocysteine lowering gene transfer strategy was evaluated in female C57BL/6 low density lipoprotein receptor (Ldlr)⁻/⁻ cystathionine-ß-synthase (Cbs)⁺/⁻ deficient mice fed a hyperhomocysteinemic and high saturated fat/high cholesterol diet using an E1E3E4-deleted hepatocyte-specific adenoviral vector expressing Cbs (AdCBS). MI was induced by permanent ligation of the left anterior descending coronary artery 14 days after saline injection or gene transfer. AdCBS gene transfer resulted in a persistent more than 5-fold (p<0.01) decrease of plasma homocysteine levels and significantly improved endothelial progenitor cell function. Selective homocysteine lowering enhanced infarct healing as indicated by a 21% (p<0.01) reduction of infarct length at day 28 after MI and by an increased number of capillaries and increased collagen content in the infarct zone. Adverse remodelling was attenuated in AdCBS MI mice as evidenced by a 29% (p<0.05) reduction of left ventricular cavity area at day 28, by an increased capillary density in the remote myocardium, and by reduced interstitial collagen. The peak rate of isovolumetric relaxation was increased by 19% (p<0.05) and the time constant of left ventricular relaxation was reduced by 21% (p<0.05) in AdCBS MI mice compared to control MI mice, indicating improved diastolic function.
    Conclusion/significance: Selective homocysteine lowering gene transfer improves infarct healing, attenuates remodelling, and significantly enhances diastolic function post-MI in female C57BL/6 Ldlr⁻/⁻ Cbs⁺/⁻ mice. The current study corroborates the view that hyperhomocysteinemia exerts direct effects on the myocardium and may potentiate the development of heart failure.
    MeSH term(s) Adenoviridae/genetics ; Animals ; Cystathionine beta-Synthase/genetics ; Cystathionine beta-Synthase/metabolism ; Diastole/physiology ; Diet, High-Fat ; Female ; Genetic Vectors ; Heart/physiopathology ; Heart Failure/genetics ; Heart Failure/pathology ; Heart Failure/physiopathology ; Heart Failure/therapy ; Homocysteine/blood ; Homocystinuria/genetics ; Homocystinuria/pathology ; Homocystinuria/physiopathology ; Homocystinuria/therapy ; Hypercholesterolemia/genetics ; Hypercholesterolemia/pathology ; Hypercholesterolemia/physiopathology ; Hypercholesterolemia/therapy ; Hyperhomocysteinemia/genetics ; Hyperhomocysteinemia/pathology ; Hyperhomocysteinemia/physiopathology ; Hyperhomocysteinemia/therapy ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardial Infarction/genetics ; Myocardial Infarction/pathology ; Myocardial Infarction/physiopathology ; Myocardial Infarction/therapy ; Receptors, LDL/deficiency ; Receptors, LDL/genetics ; Transgenes ; Ventricular Remodeling/physiology
    Chemical Substances Receptors, LDL ; Homocysteine (0LVT1QZ0BA) ; Cystathionine beta-Synthase (EC 4.2.1.22)
    Language English
    Publishing date 2013-05-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0063710
    Database MEDical Literature Analysis and Retrieval System OnLINE

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