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  • 1
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    Abstract 195: Leukemia Inhibitory Factor Stimulates Cardiac Stem Cell--Derived Cardiomyocyte Renewal After Myocardial Infarction Using a Genetic Fate-Mapping Study
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Circulation Research Vol. 111, No. suppl_1 ( 2012-08-03)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 111, No. suppl_1 ( 2012-08-03)
    Kurzfassung: Cardiac stem cells or precursor cells have the potential to regenerate cardiomyocytes, but their role in the efficacy of cardioprotective drugs remains controversial. Therefore, using a genetic fate-mapping model, we tested the hypothesis that leukemia inhibitory factor (LIF) influences cardiac stem cells and stimulates endogenous cardiomyocyte renewal after myocardial infarction (MI). We generated MerCreMer-LacZ mice in which more than 99.9% of the cardiomyocytes in the left ventricular field showed positive 5-bromo-4-chloro-3-indolyl-β-d-galactoside (Xgal) staining just after tamoxifen injection (5mg/kg/d for 2 weeks). Thus, every Xgal-negative cardiomyocyte was derived from a stem or precursor cell after tamoxifen administration. The number of Xgal-negative cardiomyocytes did not change during normal aging spanning 1 year. However, at 3 months after MI, the MI mice had more Xgal-negative cells than the control mice (57.0 ± 12.0 and 3.0 ± 2.6 cells per section, respectively; P 〈 0.01). The side population (SP) cell fraction contained label-retaining cells, which differentiated into Xgal-negative cardiomyocytes after MI. Among the cytokines secreted after MI, LIF expression increased to 130 fold in MI mice but rapidly decreased within 1 week. Therefore, we injected the LIF plasmid at the time of MI to keep blood LIF concentrations high and examined its effect on regeneration. At 1 month after MI, the MI + LIF group (118.6 ± 51.5 cells per section) had more Xgal-negative cells than the MI + PBS group (37.0 ± 5.5 cells per section; P 〈 0.05). Echocardiography showed significant recovery of fractional shortening in the LIF-treated group only. Next, we immunohistochemically analyzed the effect of LIF on SP cells. On BrdU administration at 1 week after MI, the percentages of BrdU-positive SP cells in LIF- and PBS-treated mice were 59%, and 35%, respectively, suggesting that LIF influenced SP cell proliferation. The percentages of Ki67- and phosphorylated histone-3-positive SP cells were also higher in LIF-treated mice. Taken together, LIF may stimulate stem cell-derived cardiomyocyte regeneration in part by activating SP cells. We believe our findings will help provide a novel therapeutic strategy for cardiogenesis.
    Materialart: Online-Ressource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.111.suppl_1.A195
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2012
    ZDB Id: 1467838-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
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    Abstract 250: Pericardial Grafting Of Cardiac Progenitor Cells In The Three-dimensional Thick Scaffold Improves Cardiac Function After Myocardial Infarction In Mice.
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Research Vol. 115, No. suppl_1 ( 2014-07-18)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 115, No. suppl_1 ( 2014-07-18)
    Kurzfassung: Cardiac progenitor cell (CPC) therapy for heart disease has been examined enthusiastically. However, optimal scaffolds which maintain the transplanted cells are still elusive. We used clonally expanded stem cell antigen 1-positive CPCs from adult mice and produced a three-dimensional thick scaffold (CPC-scaffold), in which CPCs were cultivated up to 2 month with self-assembling peptide RADA16-I. Addition of designer self-assembling peptide containing the active motifs of 2-unit RGD binding sequence and IGF-1 promoted three-dimensional spreading and viability of CPCs. After making myocardial infarction (MI) with left coronary artery ligation in mice, we transplanted CPC-scaffold on the surface of infarction area and confined it inside of the pericardial space by closing parietal pericardium. Four weeks after transplantation, echocardiography showed that FS of treatment group (16±10%, n=17) was higher than that of control (MI only) group (10±6.8%, n=19) (P 〈 0.05) and that LVDd of treatment group (5.4±1.0mm, n=17) was smaller than that of control group (6.2±1.1mm, n=19) (P 〈 0.05). Infarction area was significantly decreased in treatment group (46±21%, n=17), compared to control group (59±19%, n=18) (P 〈 0.05). Immunohistochemical staining for von-Willebrand factor (vWF) showed that the number of vWF-positive capillaries per mm2 in treatment group (16.8±3.2, n=5) was higher than that of control group(8.9±3.4, n=5) (P 〈 0.05). There were many of CD31-positive capillaries with or without α-smooth muscle cell actin-expressing perivascular cells in the graft area. By using fluorescent-conjugated avidin, biotin-labeled scaffold was globally detected in the graft area 1 week after transplantation, but sparsely 4weeks after, suggesting that the transplanted scaffold was biodegradable. To examine whether transplanted CPCs remain in the scaffold, we labeled CPCs with red fluorescence protein (RFP). RFP+CPCs were observed in the graft area 4 weeks after transplantation of RFP+CPC-scaffold. FISH analysis showed that sex-mismatched CPCs were globally detected in the graft area on the surface of the heart. Therefore pericardial grafting of well-vascularized and cellularized CPC-scaffold was a useful method to improve cardiac function after MI.
    Materialart: Online-Ressource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.115.suppl_1.250
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2014
    ZDB Id: 1467838-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
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    Abstract P126: Calpain Protects the Heart from Hemodynamic Stress
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Circulation Research Vol. 109, No. suppl_1 ( 2011-12-09)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 109, No. suppl_1 ( 2011-12-09)
    Kurzfassung: Although calpains are well-known Ca 2+ -dependent intracellular cysteine proteases, the pathophysiological function of calpains in the heart remains to be elucidated. Previous reports have suggested that calpains play detrimental roles to induce apoptotic or necrotic cell death in pathological Ca 2+ -overloaded conditions such as ischemia-reperfusion injury or myocardial infarction. Recent loss of function studies have suggested that calpains play important physiological roles in development, cell migration, organization of actin cytoskeleton, and plasma membrane repair. In the present study, we generated and analyzed cardiac-specific calpain 4-deficient mice (CKO) to answer unresolved questions as to in vivo function of calpains in the heart. Ubiquitous calpain is consisted of a common regulatory subunit (calpain 4) and a large catalytic subunit (calpain 1 for μ-calpain and calpain 2 for m-calpain). In agreement with previous reports, cardiac-specific deletion of calpain 4 markedly resulted in a simultaneous decrease in protein levels of calpain 1 and 2, indicating that calpain activity was almost absent in CKO hearts. CKO showed no cardiac phenotypes under basal conditions. Then, we subjected CKO and control mice (CTL) to pressure overload by means of transverse aortic constriction (TAC). One week after TAC, CKO showed left ventricle dilatation (LVDd, CKO 3.64 ± 0.2 mm versus CTL 2.66 ± 0.05 mm), and contractile dysfunction (FS, CKO 33.2 ± 3.9% versus CTL 47 ± 0.7%). CKO hearts took up Evans blue, a membrane-impermeant dye, within cardiomyocytes after TAC, whereas CTL hearts or sham-operated CKO hearts did not. This indicates plasma membrane was disrupted in CKO hearts in response to pressure overload. We performed membrane repair assays on isolated cardiomyocytes from CKO hearts using a two-photon laser-scanning microscope. CKO cardiomyocytes continued to take up FM1-43FX dye for at least 480 sec after disruption of a plasma membrane by laser irradiation, although CTL cardiomyocytes resealed within 250 sec. These data indicate that plasma membrane of cardiomyocytes disrupted by pressure overload failed to be resealed in CKO hearts. Thus, we conclude that calpains protect the heart from hemodynamic stresses by promoting membrane repair.
    Materialart: Online-Ressource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.109.suppl_1.AP126
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2011
    ZDB Id: 1467838-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
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    Acute Pressure Overload Could Induce Hypertrophic Responses in the Heart of Angiotensin II Type 1a Knockout Mice
    Ovid Technologies (Wolters Kluwer Health) ; 1998
    In:  Circulation Research Vol. 82, No. 7 ( 1998-04-20), p. 779-785
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 82, No. 7 ( 1998-04-20), p. 779-785
    Kurzfassung: Abstract —Increasing evidence has suggested that locally produced angiotensin II (Ang II) plays an important role in the development of cardiac hypertrophy through the Ang II type 1 receptor (AT1). We and others have recently reported that Ang II is critical for mechanical stress–induced hypertrophic responses in vitro. Using AT1a knockout (KO) mice, we examined whether Ang II is indispensable for pressure overload–induced cardiac hypertrophy in the present study. Reverse-transcriptase polymerase chain reaction analysis revealed that AT1 mRNA levels were 〈 10% in the heart of KO mice compared with wild-type (WT) mice, but the Ang II type 2 receptor gene was expressed at almost the same levels in the hearts of both mice. Intravenous infusion of subpressor dose of Ang II induced c- fos gene expression in the hearts of WT mice but not KO mice. Acute pressure overload, however, induced expressions of immediate-early response genes and activations of mitogen-activated protein kinases in the hearts of KO mice as well as WT mice. Both basal and activated levels of all these responses were significantly higher in KO mice than in WT mice. Pressure overload markedly increased the heart weight–to–body weight ratio in both mice strains at 14 days after aortic banding. These results suggest that acute hypertrophic responses could be induced by pressure overload in the in vivo heart without AT1 signaling.
    Materialart: Online-Ressource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.82.7.779
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 1998
    ZDB Id: 1467838-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
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    Response to the Letter by Devaux et al
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Circulation Research Vol. 113, No. 5 ( 2013-08-16)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 113, No. 5 ( 2013-08-16)
    Materialart: Online-Ressource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.113.302125
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2013
    ZDB Id: 1467838-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
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    Inhibition of Semaphorin As a Novel Strategy for Therapeutic Angiogenesis
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Circulation Research Vol. 106, No. 2 ( 2010-02-05), p. 391-398
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 106, No. 2 ( 2010-02-05), p. 391-398
    Kurzfassung: Rationale : The axon-guiding molecules known as semaphorins and their receptors (plexins) regulate the vascular pattern and play an important role in the development of vascular network during embryogenesis. Semaphorin (Sema)3E is one of the class 3 semaphorins, and plexinD1 is known to be its receptor. Although these molecules have a role in embryonic vascular development, it remains unclear whether the Sema3E/plexinD1 axis is involved in postnatal angiogenesis. Objective : The objective of this study was to elucidate the role of Sema3E/plexinD1 in postnatal angiogenesis. Methods and Results : Sema3E inhibited cell growth and tube formation by suppressing the vascular endothelial growth factor (VEGF) signaling pathway. Expression of Sema3E and plexinD1 was markedly upregulated in ischemic limbs of mice (2.5- and 4.5-fold increase for Sema3E and plexinD1, respectively), and inhibition of this pathway by introduction of the plexinD1-Fc gene or disruption of Sema3E led to a significant increase of blood flow recovery (1.6- and 1.5-fold increase for the plexinD1-Fc gene treatment and Sema3E disruption, respectively). Hypoxia activated the tumor suppressor protein p53, thereby upregulating Sema3E expression. Expression of p53 and Sema3E was enhanced in diabetic mice compared with normal mice (2- and 1.3-fold increase for p53 and Sema3E, respectively). Consequently, neovascularization after VEGF treatment was poor in the ischemic tissues of diabetic mice, whereas treatment with VEGF plus plexinD1-Fc markedly improved neovascularization. Conclusions : These results indicate that inhibition of Sema3E may be a novel strategy for therapeutic angiogenesis, especially when VEGF is ineffective.
    Materialart: Online-Ressource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.109.210815
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2010
    ZDB Id: 1467838-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
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    A Strategy for Genomic Research on Common Cardiovascular Diseases Aiming at the Realization of Precision Medicine : Personal Insights and Perspectives
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Circulation Research Vol. 119, No. 8 ( 2016-09-30), p. 900-903
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 119, No. 8 ( 2016-09-30), p. 900-903
    Materialart: Online-Ressource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.116.309802
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2016
    ZDB Id: 1467838-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 8
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    Cardiac Nonmyocytes in the Hub of Cardiac Hypertrophy
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Circulation Research Vol. 117, No. 1 ( 2015-06-19), p. 89-98
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 117, No. 1 ( 2015-06-19), p. 89-98
    Kurzfassung: Cardiac hypertrophy is characterized by complex multicellular alterations, such as cardiomyocyte growth, angiogenesis, fibrosis, and inflammation. The heart consists of myocytes and nonmyocytes, such as fibroblasts, vascular cells, and blood cells, and these cells communicate with each other directly or indirectly via a variety of autocrine or paracrine mediators. Accumulating evidence has suggested that nonmyocytes actively participate in the development of cardiac hypertrophy. In this review, recent progress in our understanding of the importance of nonmyocytes as a hub for induction of cardiac hypertrophy is summarized with an emphasis of the contribution of noncontact communication mediated by diffusible factors between cardiomyocytes and nonmyocytes in the heart.
    Materialart: Online-Ressource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.117.305349
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2015
    ZDB Id: 1467838-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 9
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    Abstract 751: The Inhibition of PARP Provides Greatercardioprotection in Mice With Heart Failure
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Circulation Research Vol. 125, No. Suppl_1 ( 2019-08-02)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 125, No. Suppl_1 ( 2019-08-02)
    Kurzfassung: The most cause of death in Japan is cancer and the second is heart disease. It is expected that the number of patients with both diseases will continue to increase in the increasingly aging society. Cardiotoxicity by anticancer agents has been recognized for a long time, for example alkylating agents, antimetabolites, proteasome inhibitors, and anthracycline anticancer agents. As cancer patients and heart failure patients increase, the number of patients suffering both diseases at the same time will naturally increase. In recent years, many new anticancer drugs have been developed and are on the market in succession, and the research on cardiotoxicity in each drug has not kept up. In 2017, from our group, there was a report that inflammation was caused by an increase in cardiomyocyte single strand breaks in pressure-overload heart failure model mice, and that inflammation contributes to declining cardiac function . DNA repair related protein PARP1 plays an important role in the repair mechanism of SSBs. PARP inhibitor disturbs its mechanism and exerts antitumor effect by causing tumor cells to become apoptosis. Therefore, we hypothesize that orally administered PARP inhibitors in heart failure patients will inhibit DNA repair by PARP, thus exacerbate inflammation and impair cardiac function more. To examine this hypothesis, we administered a representative PARP inhibitor, olaparib to pressure-overload heart failure model mice. Surprisingly, the cardiac function was improved in the olaparib administrated group. PARP is known to recruit DNA repair related proteins through synthesis of PAR (Poly-ADP-Ribose) on the DNA damage sites. In recent reports, several studies have shown that the accumulation of PAR would be involved in the worsening of the disease state in cerebellar degenerative ataxia and Parkinson's disease. In our immunostaining study of PAR using the heart tissue specimens from 58 patients with dilated cardiomyopathy, PAR was stained much more in patients with poor outcomes. I believe that PARP inhibitors may have a cardioprotective effect by preventing the accumulation of PAR, and we are now conducting further analyzes.
    Materialart: Online-Ressource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.125.suppl_1.751
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2019
    ZDB Id: 1467838-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 10
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    Abstract 489: CC Chemokine Receptor 5 Protects the Heart from Inflammation in Pressure Overload-induced Cardiac Dysfunction
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Circulation Research Vol. 125, No. Suppl_1 ( 2019-08-02)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 125, No. Suppl_1 ( 2019-08-02)
    Kurzfassung: Objective: Sustained inflammation is a key pathological process in the development of heart failure and thus suppression of inflammation possibly leads to improvement of cardiac dysfunction. It has been suggested that CC chemokine receptor 5 (CCR5) scavenges pro-inflammatory mediators and resolves inflammation. The aim of this study is to uncover the role of CCR5 in the pathogenesis of heart failure. Methods: Pressure overload heart failure was induced by transverse aortic constriction (TAC). Sham or TAC operation was performed in male 10-week-old CCR5 knockout (KO) mice and wild-type (WT) controls. Cardiac function and morphology were examined by echocardiography 1 week and 4 weeks after TAC surgery. After euthanization, the heart was extracted and embedded in paraffin for the measurements of cardiac fibrosis and cardiomyocyte hypertrophy with EVG stain and immunohistochemistry using WGA, respectively. The extent of inflammation was evaluated by the immunostaining against CD45 and F4/80 antigens, and by qRT-PCR for inflammatory cytokines and chemokines. Results: We found that heart weight was significantly larger and fractional shortening was significantly lower in CCR5 KO mice than those in WT 4 weeks after TAC, indicating CCR5-induced protective effects on heart failure development. Whilst there was no difference observed in the extent of fibrosis, the size of cardiomyocytes from CCR5 KO heart tended to be increased compared to WT. The number of CD45-positive inflammatory cells and F4/80-positive macrophage infiltration was increased 1 week after TAC in KO mice. The RNA expression levels of monocyte chemotactic protein-1, transforming growth factor-β and tumor necrosis factor-α were significantly higher and NFκB p65 was more phosphorylated in KO mice. Conclusions: We revealed that the inflammation in pressure overload-induced heart failure was exacerbated by the deletion of CCR5 and, therefore, CCR5 could contribute to resolution of inflammation and be a potential therapeutic target for the heart failure treatment.
    Materialart: Online-Ressource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.125.suppl_1.489
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2019
    ZDB Id: 1467838-X
    Standort Signatur Einschränkungen Verfügbarkeit
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