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  1. Article ; Online: Wnt11 in regulation of physiological and pathological cardiac growth.

    Halmetoja, Eveliina / Nagy, Irina / Szabo, Zoltan / Alakoski, Tarja / Yrjölä, Raisa / Vainio, Laura / Viitavaara, Eliina / Lin, Ruizhu / Rahtu-Korpela, Lea / Vainio, Seppo / Kerkelä, Risto / Magga, Johanna

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2022  Volume 36, Issue 10, Page(s) e22544

    Abstract: Wnt11 regulates early cardiac development and left ventricular compaction in the heart, but it is not known how Wnt11 regulates postnatal cardiac maturation and response to cardiac stress in the adult heart. We studied cell proliferation/maturation in ... ...

    Abstract Wnt11 regulates early cardiac development and left ventricular compaction in the heart, but it is not known how Wnt11 regulates postnatal cardiac maturation and response to cardiac stress in the adult heart. We studied cell proliferation/maturation in postnatal and adolescent Wnt11 deficient (Wnt11-/-) heart and subjected adult mice with partial (Wnt11+/-) and complete Wnt11 (Wnt11-/-) deficiency to cardiac pressure overload. In addition, we subjected primary cardiomyocytes to recombinant Wnt proteins to study their effect on cardiomyocyte growth. Wnt11 deficiency did not affect cardiomyocyte proliferation or maturation in the postnatal or adolescent heart. However, Wnt11 deficiency led to enlarged heart phenotype that was not accompanied by significant hypertrophy of individual cardiomyocytes. Analysis of stressed adult hearts from wild-type mice showed a progressive decrease in Wnt11 expression in response to pressure overload. When studied in experimental cardiac pressure overload, Wnt11 deficiency did not exacerbate cardiac hypertrophy or remodeling and cardiac function remained identical between the genotypes. When subjecting cardiomyocytes to hypertrophic stimulus, the presence of recombinant Wnt11 together with Wnt5a reduced protein synthesis. In conclusion, Wnt11 deficiency does not affect postnatal cardiomyocyte proliferation but leads to cardiac growth. Interestingly, Wnt11 deficiency alone does not substantially modulate hypertrophic response to pressure overload in vivo. Wnt11 may require cooperation with other noncanonical Wnt proteins to regulate hypertrophic response under stress.
    MeSH term(s) Animals ; Cardiomegaly/metabolism ; Cell Proliferation ; Heart/growth & development ; Mice ; Myocardium ; Myocytes, Cardiac/metabolism ; Wnt Proteins/genetics ; Wnt Proteins/metabolism
    Chemical Substances Wnt Proteins ; Wnt11 protein, mouse
    Language English
    Publishing date 2022-09-13
    Publishing country United States
    Document type Journal Article
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.202101856RRRR
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2266: Show issues Location:
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    Zs.MO 296: Show issues

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  2. Article ; Online: GSK3β Serine 389 Phosphorylation Modulates Cardiomyocyte Hypertrophy and Ischemic Injury.

    Vainio, Laura / Taponen, Saija / Kinnunen, Sini M / Halmetoja, Eveliina / Szabo, Zoltan / Alakoski, Tarja / Ulvila, Johanna / Junttila, Juhani / Lakkisto, Päivi / Magga, Johanna / Kerkelä, Risto

    International journal of molecular sciences

    2021  Volume 22, Issue 24

    Abstract: Prior studies show that glycogen synthase kinase 3β (GSK3β) contributes to cardiac ischemic injury and cardiac hypertrophy. GSK3β is constitutionally active and phosphorylation of GSK3β at serine 9 (S9) inactivates the kinase and promotes cellular growth. ...

    Abstract Prior studies show that glycogen synthase kinase 3β (GSK3β) contributes to cardiac ischemic injury and cardiac hypertrophy. GSK3β is constitutionally active and phosphorylation of GSK3β at serine 9 (S9) inactivates the kinase and promotes cellular growth. GSK3β is also phosphorylated at serine 389 (S389), but the significance of this phosphorylation in the heart is not known. We analyzed GSK3β S389 phosphorylation in diseased hearts and utilized overexpression of GSK3β carrying ser→ala mutations at S9 (S9A) and S389 (S389A) to study the biological function of constitutively active GSK3β in primary cardiomyocytes. We found that phosphorylation of GSK3β at S389 was increased in left ventricular samples from patients with dilated cardiomyopathy and ischemic cardiomyopathy, and in hearts of mice subjected to thoracic aortic constriction. Overexpression of either GSK3β S9A or S389A reduced the viability of cardiomyocytes subjected to hypoxia-reoxygenation. Overexpression of double GSK3β mutant (S9A/S389A) further reduced cardiomyocyte viability. Determination of protein synthesis showed that overexpression of GSK3β S389A or GSK3β S9A/S389A increased both basal and agonist-induced cardiomyocyte growth. Mechanistically, GSK3β S389A mutation was associated with activation of mTOR complex 1 signaling. In conclusion, our data suggest that phosphorylation of GSK3β at S389 enhances cardiomyocyte survival and protects from cardiomyocyte hypertrophy.
    MeSH term(s) Animals ; Cardiomegaly/metabolism ; Cardiomegaly/pathology ; Cell Proliferation ; Cell Survival ; Cells, Cultured ; Glycogen Synthase Kinase 3 beta/metabolism ; Humans ; Male ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mice ; Mice, Inbred C57BL ; Myocardial Ischemia/metabolism ; Myocardial Ischemia/pathology ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Phosphorylation ; Rats, Sprague-Dawley ; Rats
    Chemical Substances GSK3B protein, human (EC 2.7.11.1) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Gsk3b protein, mouse (EC 2.7.11.1) ; Gsk3b protein, rat (EC 2.7.11.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
    Language English
    Publishing date 2021-12-18
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms222413586
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: MiR-185-5p regulates the development of myocardial fibrosis.

    Lin, Ruizhu / Rahtu-Korpela, Lea / Szabo, Zoltan / Kemppi, Anna / Skarp, Sini / Kiviniemi, Antti M / Lepojärvi, E Samuli / Halmetoja, Eveliina / Kilpiö, Teemu / Porvari, Katja / Pakanen, Lasse / Tolva, Johanna / Paakkanen, Riitta / Segersvärd, Heli / Tikkanen, Ilkka / Laine, Mika / Sinisalo, Juha / Lakkisto, Päivi / Huikuri, Heikki /
    Magga, Johanna / Junttila, Juhani / Kerkelä, Risto

    Journal of molecular and cellular cardiology

    2021  Volume 165, Page(s) 130–140

    Abstract: Background: Cardiac fibrosis stiffens the ventricular wall, predisposes to cardiac arrhythmias and contributes to the development of heart failure. In the present study, our aim was to identify novel miRNAs that regulate the development of cardiac ... ...

    Abstract Background: Cardiac fibrosis stiffens the ventricular wall, predisposes to cardiac arrhythmias and contributes to the development of heart failure. In the present study, our aim was to identify novel miRNAs that regulate the development of cardiac fibrosis and could serve as potential therapeutic targets for myocardial fibrosis.
    Methods and results: Analysis for cardiac samples from sudden cardiac death victims with extensive myocardial fibrosis as the primary cause of death identified dysregulation of miR-185-5p. Analysis of resident cardiac cells from mice subjected to experimental cardiac fibrosis model showed induction of miR-185-5p expression specifically in cardiac fibroblasts. In vitro, augmenting miR-185-5p induced collagen production and profibrotic activation in cardiac fibroblasts, whereas inhibition of miR-185-5p attenuated collagen production. In vivo, targeting miR-185-5p in mice abolished pressure overload induced cardiac interstitial fibrosis. Mechanistically, miR-185-5p targets apelin receptor and inhibits the anti-fibrotic effects of apelin. Finally, analysis of left ventricular tissue from patients with severe cardiomyopathy showed an increase in miR-185-5p expression together with pro-fibrotic TGF-β1 and collagen I.
    Conclusions: Our data show that miR-185-5p targets apelin receptor and promotes myocardial fibrosis.
    MeSH term(s) Animals ; Apelin Receptors/metabolism ; Cardiomyopathies/metabolism ; Collagen/metabolism ; Fibroblasts/metabolism ; Fibrosis ; Humans ; Mice ; MicroRNAs/metabolism
    Chemical Substances Apelin Receptors ; MIRN185 microRNA, human ; MicroRNAs ; Mirn185 microRNA, mouse ; Collagen (9007-34-5)
    Language English
    Publishing date 2021-12-29
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80157-4
    ISSN 1095-8584 ; 0022-2828
    ISSN (online) 1095-8584
    ISSN 0022-2828
    DOI 10.1016/j.yjmcc.2021.12.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 426: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  4. Article ; Online: Characterization of apela, a novel endogenous ligand of apelin receptor, in the adult heart.

    Perjés, Ábel / Kilpiö, Teemu / Ulvila, Johanna / Magga, Johanna / Alakoski, Tarja / Szabó, Zoltán / Vainio, Laura / Halmetoja, Eveliina / Vuolteenaho, Olli / Petäjä-Repo, Ulla / Szokodi, István / Kerkelä, Risto

    Basic research in cardiology

    2016  Volume 111, Issue 1, Page(s) 2

    Abstract: The G protein-coupled apelin receptor regulates important processes of the cardiovascular homeostasis, including cardiac development, cardiac contractility, and vascular tone. Most recently, a novel endogenous peptide ligand for the apelin receptor was ... ...

    Abstract The G protein-coupled apelin receptor regulates important processes of the cardiovascular homeostasis, including cardiac development, cardiac contractility, and vascular tone. Most recently, a novel endogenous peptide ligand for the apelin receptor was identified in zebrafish, and it was named apela/elabela/toddler. The peptide was originally considered as an exclusively embryonic regulator, and so far its function in the adult organism remains elusive. We show here that apela is predominantly expressed in the non-cardiomyocyte fraction in the adult rodent heart. We also provide evidence that apela binds to apelin receptors in the heart. Using isolated adult rat hearts, we demonstrate, that just like the fellow receptor agonist apelin, apela increases cardiac contractility and induces coronary vasodilation already in the nanomolar level. The inotropic effect, as revealed by Western blot analysis, is accompanied by a significant increase in extracellular signal-regulated kinase (ERK) 1/2 phosphorylation. Pharmacological inhibition of ERK1/2 activation markedly attenuates the apela-induced inotropy. Analysis of samples from infarcted mouse hearts showed that expression of both apela and apelin receptor is induced in failing mouse hearts and correlate with left ventricular ejection fraction. Hence, we conclude that apela is present in the adult heart, is upregulated in post-infarction cardiac remodeling, and increases cardiac contractility in an ERK1/2-dependent manner.
    MeSH term(s) Aging ; Animals ; Apelin Receptors ; Blotting, Western ; Disease Models, Animal ; Heart ; Intercellular Signaling Peptides and Proteins/metabolism ; Male ; Mice ; Myocardial Infarction/metabolism ; Myocardium/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, G-Protein-Coupled/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/physiology
    Chemical Substances Apelin Receptors ; Aplnr protein, mouse ; Aplnr protein, rat ; Intercellular Signaling Peptides and Proteins ; Receptors, G-Protein-Coupled
    Language English
    Publishing date 2016-01
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 189755-x
    ISSN 1435-1803 ; 0300-8428 ; 0175-9418
    ISSN (online) 1435-1803
    ISSN 0300-8428 ; 0175-9418
    DOI 10.1007/s00395-015-0521-6
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