Cellular and Molecular Mechanisms Underlying Lps-associated Myocyte Impairment.
From: Dept. of Physiology and Biophysics, Univ. of Calgary Medical Centre, AB, Canada.
American journal of physiology. Heart and circulatory physiology
- Publish Date: Feb 2006
- ISSN: 0363-6135
- Volume: 290
- Issue: 2
- Pages: H800-6
- Medium: Print
- Language: English
- Citation (JAMA): Tavener Samantha A, Kubes Paul, et al. Cellular and Molecular Mechanisms Underlying Lps-associated Myocyte Impairment.. Am. J. Physiol. Heart Circ. Physiol. Feb 2006;290:H800-6
Abstract
Recently we reported that Toll-like receptor 4 (TLR4)-positive immune cells of unknown identity were responsible for the LPS-induced depression of cardiac myocyte shortening. The aim of this study is to identify the TLR4-positive cell type that is responsible for the LPS-induced cardiac dysfunction. Neither neutrophil depletion alone nor mast cell deficiency had any impact on the impairment of myocyte shortening during LPS treatment. In contrast, LPS-treated, macrophage-deficient mice demonstrated a partial reduction in shortening compared with saline-treated, macrophage-deficient mice. Because the removal of macrophages could only partially restore myocyte shortening, we also investigated the effects of removing both neutrophils and macrophages on myocyte shortening. Interestingly, endotoxemic, neutrophil-depleted, and macrophage-deficient mice had completely restored myocyte shortening. Because both macrophages and neutrophils can produce nitric oxide (NO) and TNF-alpha, we examined LPS-treated inducible NO synthase knockout (iNOSKO) mice and TNF receptor (TNFR)-deficient mice. Eliminating both TNFR1 and TNFR2 was required to restore myocyte shortening during LPS treatment, whereas iNOS deficiency had no effect. These data suggest that macrophages and to a lesser degree neutrophils cause cardiac impairment, presumably via TNF-alpha.
Mesh Headings (Keywords): Animals, Endotoxemia, Heart Ventricles, Lipopolysaccharides, Macrophages, Male, Mast Cells, Mice, Mice, Inbred C57BL, Mice, Knockout, Myocardial Contraction, Myocytes, Cardiac, Neutrophils, Nitric Oxide, Nitric Oxide Synthase Type II, Receptors, Tumor Necrosis Factor, Type I, Receptors, Tumor Necrosis Factor, Type II, Toll-Like Receptor 4, Tumor Necrosis Factor-alpha
Check for Full Text / PubMed Unique Identifier (PMID): 16172157
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