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  • 1 Duke University Medical Center Department of Pathology Durham NC 27710 USA
  • | 2 National Heart, Lung, Blood Institute, NIH Translational Medicine Branch Bethesda MD 20892 USA
  • | 3 David Geffen School of Medicine at UCLA Los Angeles Departments of Anesthesiology and Medicine California 90095 USA
  • | 4 Johns Hopkins University Department of Pathology Baltimore MD 21205 USA
  • | 5 Johns Hopkins University Department of Pathology 720 Rutland Avenue, Ross 632N Baltimore MD 21205 USA
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The p38 MAP kinases are stress-activated MAP kinases whose induction is often associated with the onset of heart failure. This study investigated the role of p38 MAP kinase isoforms in the regulation of myocardial contractility and ischemia/reperfusion injury using mice with cardiac-specific expression of kinase dead (dominant negative) mutants of p38α (p38αdn) or p38β (p38βdn). Hearts were subjected to 20 min ischemia and 40 min reperfusion. Immunofluorescence staining for p38αdn and p38βdn protein was performed on neonatal cardiomyocytes infected with adenovirus expressing flag-tagged p38αdn and p38βdn protein. Basal contractile function was increased in both p38αdn and p38βdn hearts compared to WT. Ischemic injury was increased in p38βdn vs. WT hearts, as indicated by lower posti-schemic recoveries of contractile function and ATP. However, despite a similar increase in contractility, ischemic injury was not increased in p38αdn vs. WT hearts. Immunohistological analysis of cardiomyocytes with comparable levels of protein overexpression show that p38αdn and p38βdn proteins were co-localized with sarcomeric α-actinin, however, p38αdn was detected in the nucleus while p38βdn was exclusively detected in the cytosol. In summary, attenuated p38 activity led to increased myocardial contractility; specific isoforms of p38 and their sub-cellular localization may have different roles in modulating ischemic injury.

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Senior editors

Editor(s)-in-Chief: Rosivall, László

Honorary Editor(s)-in-Chief): Monos, Emil

Managing Editor(s): Bartha, Jenő; Berhidi, Anna

Co-editor(s): Koller, Ákos; Lénárd, László; Szénási, Gábor

Assistant Editor(s): G. Dörnyei (Budapest), Zs. Miklós (Budapest), Gy. Nádasy (Budapest)

Hungarian Editorial Board

      Benedek, György (Szeged)
      Benyó, Zoltán (Budapest)
      Boros, Mihály (Szeged)
      Chernoch, László (Debrecen)
      Détári, László (Budapest)
      Hamar, János (Budapest)
      Hantos, Zoltán (Szeged)
      Hunyady, László (Budapest)
      Imre, Sándor (Debrecen)
      Jancsó, Gábor (Szeged)
      Karádi, Zoltán (Pécs)
      Kovács, László (Debrecen)
      Palkovits, Miklós (Budapest)
      Papp, Gyula (Szeged)
      Pavlik, Gábor (Budapest)
      Spät, András (Budapest)
      Szabó, Gyula (Szeged)
      Szelényi, Zoltán (Pécs)
      Szolcsányi, János (Pécs)
      Szollár, Lajos (Budapest)
      Szücs, Géza (Debrecen)
      Telegdy, Gyula (Szeged)
      Toldi, József (Szeged)
      Tósaki, Árpád (Debrecen)

International Editorial Board

      R. Bauer (Jena)
      W. Benjelloun (Rabat)
      A. W. Cowley Jr. (Milwaukee)
      D. Djuric (Belgrade)
      C. Fry (London)
      S. Greenwald (London)
      O. Hänninen (Kuopio)
      H. G. Hinghofer-Szalkay (Graz)
      Th. Kenner (Graz)
      Gy. Kunos (Richmond)
      M. Mahmoudian (Tehran)
      T. Mano (Seki, Gifu)
      G. Navar (New Orleans)
      H. Nishino (Nagoya)
      O. Petersen (Liverpool)
      U. Pohl (Münich)
      R. S. Reneman (Maastricht)
      A. Romanovsky (Phoenix)
      G. M. Rubanyi (Richmond)
      T. Sakata (Oita)
      A. Siddiqui (Karachi)
      Cs. Szabo (Beverly)
      E. Vicaut (Paris)
      N. Westerhof (Amsterdam)
      L. F. Zhang (Xi'an)

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Acta Physiologica Hungarica
Language English
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1950
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Founder Magyar Tudományos Akadémia
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ISSN 0231-424X (Print)
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