Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Alerts
  • Advertising/recruitment
  • Subscribe
  • Contact
  • Current Issue
  • Past Issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews ...
    • 100th Anniversary of Insulin's Discovery (Jan 2021)
    • Hypoxia-inducible factors in disease pathophysiology and therapeutics (Oct 2020)
    • Latency in Infectious Disease (Jul 2020)
    • Immunotherapy in Hematological Cancers (Apr 2020)
    • Big Data's Future in Medicine (Feb 2020)
    • Mechanisms Underlying the Metabolic Syndrome (Oct 2019)
    • Reparative Immunology (Jul 2019)
    • View all review series ...
  • Viewpoint
  • Collections
    • Recently published
    • In-Press Preview
    • Commentaries
    • Concise Communication
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • In-Press Preview
  • Commentaries
  • Concise Communication
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Alerts
  • Advertising/recruitment
  • Subscribe
  • Contact
Top
  • View PDF
  • Download citation information
  • Send a letter
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need Help? E-mail the JCI
  • Top
  • Abstract
  • Version history
  • Article usage
  • Citations to this article

Advertisement

Research Article Free access | 10.1172/JCI117865

Transgenic mice expressing the human heat shock protein 70 have improved post-ischemic myocardial recovery.

J C Plumier, B M Ross, R W Currie, C E Angelidis, H Kazlaris, G Kollias, and G N Pagoulatos

Department of Anatomy and Neurobiology, Dalhousie University, Halifax, Nova Scotia, Canada.

Find articles by Plumier, J. in: JCI | PubMed | Google Scholar

Department of Anatomy and Neurobiology, Dalhousie University, Halifax, Nova Scotia, Canada.

Find articles by Ross, B. in: JCI | PubMed | Google Scholar

Department of Anatomy and Neurobiology, Dalhousie University, Halifax, Nova Scotia, Canada.

Find articles by Currie, R. in: JCI | PubMed | Google Scholar

Department of Anatomy and Neurobiology, Dalhousie University, Halifax, Nova Scotia, Canada.

Find articles by Angelidis, C. in: JCI | PubMed | Google Scholar

Department of Anatomy and Neurobiology, Dalhousie University, Halifax, Nova Scotia, Canada.

Find articles by Kazlaris, H. in: JCI | PubMed | Google Scholar

Department of Anatomy and Neurobiology, Dalhousie University, Halifax, Nova Scotia, Canada.

Find articles by Kollias, G. in: JCI | PubMed | Google Scholar

Department of Anatomy and Neurobiology, Dalhousie University, Halifax, Nova Scotia, Canada.

Find articles by Pagoulatos, G. in: JCI | PubMed | Google Scholar

Published April 1, 1995 - More info

Published in Volume 95, Issue 4 on April 1, 1995
J Clin Invest. 1995;95(4):1854–1860. https://doi.org/10.1172/JCI117865.
© 1995 The American Society for Clinical Investigation
Published April 1, 1995 - Version history
View PDF
Abstract

Heat shock treatment induces expression of several heat shock proteins and subsequent post-ischemic myocardial protection. Correlations exist between the degree of stress used to induce the heat shock proteins, the amount of the inducible heat shock protein 70 (HSP70) and the level of myocardial protection. The inducible HSP70 has also been shown to be protective in transfected myogenic cells. Here we examined the role of human inducible HSP70 in transgenic mouse hearts. Overexpression of the human HSP70 does not appear to affect normal protein synthesis or the stress response in transgenic mice compared with nontransgenic mice. After 30 min of ischemia, upon reperfusion, transgenic hearts versus nontransgenic hearts showed significantly improved recovery of contractile force (0.35 +/- 0.08 versus 0.16 +/- 0.05 g, respectively, P < 0.05), rate of contraction, and rate of relaxation. Creatine kinase, an indicator of cellular injury, was released at a high level (67.7 +/- 23.0 U/ml) upon reperfusion from nontransgenic hearts, but not transgenic hearts (1.6 +/- 0.8 U/ml). We conclude that high level constitutive expression of the human inducible HSP70 plays a direct role in the protection of the myocardium from ischemia and reperfusion injury.

Images.

Browse pages

Click on an image below to see the page. View PDF of the complete article

icon of scanned page 1854
page 1854
icon of scanned page 1855
page 1855
icon of scanned page 1856
page 1856
icon of scanned page 1857
page 1857
icon of scanned page 1858
page 1858
icon of scanned page 1859
page 1859
icon of scanned page 1860
page 1860
Version history
  • Version 1 (April 1, 1995): No description

Article tools

  • View PDF
  • Download citation information
  • Send a letter
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need Help? E-mail the JCI

Metrics

  • Article usage
  • Citations to this article

Go to

  • Top
  • Abstract
  • Version history
Advertisement
Advertisement
Follow JCI:
Copyright © 2021 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts