Burn trauma alters calcium transporter protein expression in the heart

Cherry Ballard-Croft, Deborah Carlson, David L. Maass, Jureta W. Horton

Research output: Contribution to journalArticlepeer-review

27 Scopus citations

Abstract

We have shown previously that burn trauma produces significant cardiac dysfunction, which is first evident 8 h postburn and is maximal 24 h postburn. Because calcium handling by the cardiomyocyte is essential for cardiac function, one mechanism by which burn injury may cause cardiac abnormalities is via calcium dyshomeostasis. We hypothesized that major burn injury alters cardiomyocyte calcium handling through changes in calcium transporter expression. Sprague-Dawley rats were given either burn injury or no burn injury (controls). Cardiomyocyte intracellular calcium and sodium were quantified at various times postburn by fura 2-AM or sodium-binding benzofuran isophthalate fluorescent indicators, respectively. In addition, hearts freeze-clamped at various times postburn (2, 4, 8, and 24 h) were used for Western blot analysis using antibodies against the sarcoplasmic reticulum calcium-ATPase (SERCA), the L-type calcium-channel, the ryanodine receptor, the sodium/calcium exchanger, or the sodium-potassium-ATPase. Intracellular calcium levels were elevated significantly 8-24 h postburn, and intracellular sodium was increased significantly 4 through 24 h postburn. Expression of SERCA was significantly reduced 1-8 h postburn, whereas L-type calcium-channel expression was diminished 1 and 2 h postburn (P < 0.05) but returned toward control levels 4 h postburn. Ryanodine receptor protein was significantly reduced at 1 and 2 h postburn, returning to baseline by 4 h postburn. Sodium/calcium exchanger expression was significantly elevated 2 h postburn but was significantly reduced 24 h postburn. An increase in sodium-potassium-ATPase expression occurred 2-24 h postburn. These data confirm that burn trauma alters calcium transporter expression, likely contributing to cardiomyocyte calcium loading and cardiac contractile dysfunction.

Original languageEnglish
Pages (from-to)1470-1476
Number of pages7
JournalJournal of Applied Physiology
Volume97
Issue number4
DOIs
StatePublished - Oct 2004

Funding

FundersFunder number
National Institute of General Medical SciencesR01GM057054

    Keywords

    • Cardiomyocyte calcium
    • Cardiomyocyte sodium
    • Fluorescent indicators
    • Fura 2-AM/SBFI
    • Rat model of thermal injury

    ASJC Scopus subject areas

    • General Medicine

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