• Login
    View Item 
    •   UMB Digital Archive
    • UMB Open Access Articles
    • UMB Open Access Articles
    • View Item
    •   UMB Digital Archive
    • UMB Open Access Articles
    • UMB Open Access Articles
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of UMB Digital ArchiveCommunitiesPublication DateAuthorsTitlesSubjectsThis CollectionPublication DateAuthorsTitlesSubjects

    My Account

    LoginRegister

    Statistics

    Display statistics

    MK2-Deficient Mice Are Bradycardic and Display Delayed Hypertrophic Remodeling in Response to a Chronic Increase in Afterload.

    • CSV
    • RefMan
    • EndNote
    • BibTex
    • RefWorks
    Author
    Ruiz, Matthieu
    Khairallah, Maya
    Dingar, Dharmendra
    Vaniotis, George
    Khairallah, Ramzi J
    Lauzier, Benjamin
    Thibault, Simon
    Trépanier, Joëlle
    Shi, Yanfen
    Douillette, Annie
    Hussein, Bahira
    Nawaito, Sherin Ali
    Sahadevan, Pramod
    Nguyen, Albert
    Sahmi, Fatiha
    Gillis, Marc-Antoine
    Sirois, Martin G
    Gaestel, Matthias
    Stanley, William C
    Fiset, Céline
    Tardif, Jean-Claude
    Allen, Bruce G
    Show allShow less

    Date
    2021-02-03
    Journal
    Journal of the American Heart Association
    Publisher
    American Heart Association Inc.
    Type
    Article
    
    Metadata
    Show full item record
    See at
    https://doi.org/10.1161/JAHA.120.017791
    Abstract
    Background Mitogen-activated protein kinase-activated protein kinase-2 (MK2) is a protein serine/threonine kinase activated by p38α/β. Herein, we examine the cardiac phenotype of pan MK2-null (MK2-/-) mice. Methods and Results Survival curves for male MK2+/+ and MK2-/- mice did not differ (Mantel-Cox test, P=0.580). At 12 weeks of age, MK2-/- mice exhibited normal systolic function along with signs of possible early diastolic dysfunction; however, aging was not associated with an abnormal reduction in diastolic function. Both R-R interval and P-R segment durations were prolonged in MK2-deficient mice. However, heart rates normalized when isolated hearts were perfused ex vivo in working mode. Ca2+ transients evoked by field stimulation or caffeine were similar in ventricular myocytes from MK2+/+ and MK2-/- mice. MK2-/- mice had lower body temperature and an age-dependent reduction in body weight. mRNA levels of key metabolic genes, including Ppargc1a, Acadm, Lipe, and Ucp3, were increased in hearts from MK2-/- mice. For equivalent respiration rates, mitochondria from MK2-/- hearts showed a significant decrease in Ca2+ sensitivity to mitochondrial permeability transition pore opening. Eight weeks of pressure overload increased left ventricular mass in MK2+/+ and MK2-/- mice; however, after 2 weeks the increase was significant in MK2+/+ but not MK2-/- mice. Finally, the pressure overload-induced decrease in systolic function was attenuated in MK2-/- mice 2 weeks, but not 8 weeks, after constriction of the transverse aorta. Conclusions Collectively, these results implicate MK2 in (1) autonomic regulation of heart rate, (2) cardiac mitochondrial function, and (3) the early stages of myocardial remodeling in response to chronic pressure overload.
    Keyword
    MK2
    bradycardia
    cardiac remodeling
    mitochondrial permeability transition pore
    p38 MAPK
    Identifier to cite or link to this item
    http://hdl.handle.net/10713/14824
    ae974a485f413a2113503eed53cd6c53
    10.1161/JAHA.120.017791
    Scopus Count
    Collections
    UMB Open Access Articles

    entitlement

    Related articles

    • MAPK-activated protein kinase-2 in cardiac hypertrophy and cyclooxygenase-2 regulation in heart.
    • Authors: Streicher JM, Ren S, Herschman H, Wang Y
    • Issue date: 2010 Apr 30
    • MK5 haplodeficiency attenuates hypertrophy and preserves diastolic function during remodeling induced by chronic pressure overload in the mouse heart.
    • Authors: Nawaito SA, Dingar D, Sahadevan P, Hussein B, Sahmi F, Shi Y, Gillis MA, Gaestel M, Tardif JC, Allen BG
    • Issue date: 2017 Jul 1
    • MAPKAPK-2 modulates p38-MAPK localization and small heat shock protein phosphorylation but does not mediate the injury associated with p38-MAPK activation during myocardial ischemia.
    • Authors: Gorog DA, Jabr RI, Tanno M, Sarafraz N, Clark JE, Fisher SG, Cao XB, Bellahcene M, Dighe K, Kabir AM, Quinlan RA, Kato K, Gaestel M, Marber MS, Heads RJ
    • Issue date: 2009 Sep
    • MK5 haplodeficiency decreases collagen deposition and scar size during post-myocardial infarction wound repair.
    • Authors: Nawaito SA, Sahadevan P, Clavet-Lanthier MÉ, Pouliot P, Sahmi F, Shi Y, Gillis MA, Lesage F, Gaestel M, Sirois MG, Calderone A, Tardif JC, Allen BG
    • Issue date: 2019 Jun 1
    • Overexpression of A kinase interacting protein 1 attenuates myocardial ischaemia/reperfusion injury but does not influence heart failure development.
    • Authors: Booij HG, Yu H, De Boer RA, van de Kolk CW, van de Sluis B, Van Deursen JM, Van Gilst WH, Silljé HH, Westenbrink BD
    • Issue date: 2016 Aug 1
    DSpace software (copyright © 2002 - 2023)  DuraSpace
    Quick Guide | Policies | Contact Us | UMB Health Sciences & Human Services Library
    Open Repository is a service operated by 
    Atmire NV
     

    Export search results

    The export option will allow you to export the current search results of the entered query to a file. Different formats are available for download. To export the items, click on the button corresponding with the preferred download format.

    By default, clicking on the export buttons will result in a download of the allowed maximum amount of items.

    To select a subset of the search results, click "Selective Export" button and make a selection of the items you want to export. The amount of items that can be exported at once is similarly restricted as the full export.

    After making a selection, click one of the export format buttons. The amount of items that will be exported is indicated in the bubble next to export format.