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Stress activated cytokines and the heart

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Abstract

The ability of myocardium to successfully compensate for, and adapt to, stress ultimately determines whether the heart will decompensate and fail, or whether it will instead maintain preserved function. Despite the importance of the myocardial response to environmental stress, very little is known with respect to the biochemical mechanisms that are responsible for mediating and integrating the stress response in the heart. In the present review we will summarize recent experimental material which suggests that cytokines that are expressed within the myocardium in response to a environment injury, namely tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1) and interleukin-6 (IL-6), may play an important role in initiating and integrating homeostatic responses within the heart. However, these ‘stress-activated’ cytokines all have the potential to produce cardiac decompensation when expressed at sufficiently high concentrations. Accordingly, the theme that will emerge from this discussion is that the short-term expression of stress-activated cytokines within the heart may provide the heart with an adaptive response to stress, whereas long-term expression of these molecules may be frankly maladaptive by producing cardiac decompensation.

References (126)

  • A Mauviel et al.

    Comparative effects of interleukin-1 and tumor necrosis factor-α on collagen production and corresponding procollagen mRNA levels in human dermal fibroblasts

    J Invest Dermatol

    (1991)
  • J.D. Hosenpud

    The effects of interleukin-I on myocardial function and metabolism

    Clin Immunol Immunopathol

    (1993)
  • C.F. Nathan et al.

    Nitric oxide synthases: roles, tolls, and controls

    Cell

    (1994)
  • P.F. Mery et al.

    Nitric oxide regulates Ca2+ current

    J Biol Chem

    (1993)
  • A.M. Shah et al.

    Effects of 8-bromo-GMP on contraction and on inotropic response of ferret cardiac muscle

    J Mol Cell Cardiol

    (1991)
  • R.N. Kolesnick

    Sphingomyelin and derivative as cellular signals

    Prog Lipid Res

    (1991)
  • R.N. Kolesnick et al.

    The sphingomyelin pathway in tumor necrosis factor and interleukin-1 signaling

    Cell

    (1994)
  • R.A. Sabbadini et al.

    Sphingosine is endogenous to cardiac and skeletal muscle

    Biochem Biophys Res Commun

    (1993)
  • R.A. Sabbadini et al.

    The effects of sphingosine on sarcoplasmic reticulum membrane calcium release

    J Biol Chem

    (1992)
  • C.A. Dettbarn et al.

    Modulation of cardiac sarcoplasmic reticulum ryanodine receptor by sphingosine

    J Mol Cell Cardiol

    (1994)
  • F Yanaga et al.

    Tumor necrosis factor α stimulates sphingomyelinase through the 55 kDa receptor in HL-60 cells

    FEBS Lett

    (1992)
  • K Wiegmann et al.

    Human 55-kDa receptor for tumor necrosis factor coupled to signal transduction cascades

    J Biol Chem

    (1992)
  • G.L. Hammond et al.

    Molecular signals for initiating protein synthesis in organ hypertrophy

  • G.L. Hammond et al.

    The molecules that initiate cardiac hypertrophy are not species specific

    Science

    (1982)
  • W Cascells et al.

    Isolation, characterization, and localization of heparin-binding growth factors in the heart

    J Clin Invest

    (1990)
  • M Eghbali

    Cellular origin and distribution of transforming growth factor-β in the normal rate myocardium

    Tissue Res

    (1989)
  • H.L. Weiner et al.

    Acidic fibroblast growth factor mRNA is expressed by cardiac myocytes in culture and the protein is localized to the extracellular matrix

  • C.S. Long et al.

    A growth factor for cardiac myocytes is produced by cardiac nonmyocytes

    Cell Regul

    (1991)
  • W Schorb et al.

    Angiotensin II is mitogenic in neonatal rat cardiac fibroblasts

    Circ Res

    (1993)
  • J.I. Sadoshima et al.

    Molecular characterization of angiotensin II-induced hypertrophy of cardiac myocytes and hyperplasia of cardiac fibroblasts

  • H Ito et al.

    Endothelin-1 is an autocrine/paracrine factor in the mechanism of angiotensin-II-induced hypertrophy in cultured rat cardiomyocytes

    J Clin Invest

    (1993)
  • H Ito et al.

    Endothelin-1 induces hypertrophy with enhanced expression of muscle specific genes in cultured neonatal rat cardiomyocytes

    Circ Res

    (1991)
  • T.G. Parker et al.

    Peptide growth factors can provoke “fetal” contractile protein gene expression in rat cardiac myocytes

    J Clin Invest

    (1990)
  • Z.L. Sheng et al.

    Cardiotrophin-1 displays early expression in the murine heart tube and promotes cardiac myocyte survival

    Development

    (1996)
  • D Pennica et al.

    Expression cloning of cardiotrophin 1, a cytokine that induces cardiac myocyte hypertrophy

  • S Kapadia et al.

    Tumor necrosis factor gene and protein expression in adult feline myocardium after endotoxin adminstration

    J Clin Invest

    (1995)
  • S Kapadia et al.

    Hemodynamic regulation of tumor necrosis factor-α gene and protein expression in adult mammalian myocardium

    Circulation

    (1995)
  • D Caput et al.

    Identification of a common nucleotide sequence in the 3′-untranslated region of mRNA molecules specifying inflammatory mediators

  • B.P. Giroir et al.

    The tissue distribution of tumor necrosis factor biosynthesis during endotoxemia

    J Clin Invest

    (1992)
  • K Yamauchi-Takihara et al.

    Hypoxic stress induces cardiac myocyte-derived interleukin-6

    Circulation

    (1995)
  • G.L. Kukielka et al.

    Induction of interleukin-6 synthesis in the myocardium

  • I Low-Friedrich et al.

    Cytokines induce stress protein formation in cultured cardiac myocytes

    Basic Res Cardiol

    (1992)
  • J.N. Palmer et al.

    Interleukin-1β induces cardiac myocyte growth but inhibits cardiac fibroblast proliferation in culture

    J Clin Invest

    (1995)
  • D.A. Raftos et al.

    Invertebrate cytokines: tunicate cell proliferation stimulated by an interleukin 1-like molecule

  • G.H.W. Wong et al.

    Induction of manganous superoxide dismutase by tumor necrosis factor: possible protective mechanism

    Science

    (1988)
  • W.K. Nelson et al.

    Leukaemia inhibitory factor and tumor necrosis factor induce manganese superoxide dismutase and protect rabbit hearts from reperfusion injury

    J Mol Cell Cardiol

    (1995)
  • M Nakano et al.

    Tumor necrosis factor-α induced expression of heat shock protein 72 in adult feline cardiac myocytes

    Am J Physiol

    (1996)
  • J.M. Brown et al.

    Interleukin I pretreatment decreases ischemia /reperfusion injury

  • M.S. Marber et al.

    Overexpression of the rat inducible 70-kd heart stress protein in a transgenic mouse increases the resistance of the heart to ischemia injury

    J Clin Invest

    (1995)
  • J.C.L. Plumier et al.

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

    J Clin Invest

    (1995)
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