Increased cardiac mast cell density and mediator release in patients with dilated cardiomyopathy

Patella, Vincenzo; Crescenzo, Gennaro de; Lamparter-Schummert, B.; Rosa, Gianluca De; Adt, M.; Marone, Gianni

doi:10.1007/s000110050041

Cited by 43 publications

(33 citation statements)

References 7 publications

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“…This changed with the advent of several studies reporting increases in cardiac mast cell density secondary to various myocardial pathologies [5,9,10,17,18]. These cardiac mast cells have been shown to be of the connective tissue type, containing a variety of biologically active mediators including cytokines and proteases that have the ability to activate MMPs.…”

Section: Discussionmentioning

confidence: 99%

“…Less well recognized is the role that cardiac mast cells play in the adverse remodeling responses of the left ventricle (LV) induced in the heart subjected to chronic elevations in myocardial stress, such as seen in heart failure [5][6][7][8], myocardial infarction [9], dilated cardiomyopathy [10] and mitral valve regurgitation [11]. Previous reports from our laboratory have provided substantial evidence supporting the role of cardiac mast cells in mediating matrix metalloproteinase (MMP) activation, which is responsible in turn for extracellular collagen matrix degradation and subsequent ventricular dilatation [5,8,12,13].…”

Section: Introductionmentioning

confidence: 99%

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Protection from adverse myocardial remodeling secondary to chronic volume overload in mast cell deficient rats

Levick

Gardner

Holland

et al. 2008

Journal of Molecular and Cellular Cardiology

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Mast cells have diverse roles throughout the body as evidenced by their heterogeneous nature. In the heart, cardiac mast cells have been implicated in left ventricular (LV) remodeling in response to elevated myocardial stress. Accordingly, the purpose of this study was to use mast cell deficient rats (Ws/Ws) to delineate the interaction between cardiac mast cell activation and LV remodeling. LV matrix metalloproteinase (MMP) activity, fibrillar collagen, TNF-α levels, and LV diameter were compared in Ws/Ws and wild type (WT) rats subjected to 5 d (n=3/group) and 8 wks (n=4/ group) of aortocaval fistula-induced volume overload. In contrast to attenuation of myocardial remodeling in the Ws/Ws group: 1) MMP-2 activity was significantly increased in the WT group at 5 d; 2) there was marked degradation of the extracellular collagen matrix in WT at 5 d and 8 wks; 3) the percent increase in LV diameter from baseline was significantly greater in WT at 2, 4, 6, and 8 wks post-fistula; and 4) myocardial TNF-α levels were markedly elevated in the WT group at 5 days post-fistula. These results underscore the importance of cardiac mast cells in mediating MMP activation, collagen degradation and LV dilatation and suggest that mast cellderived TNF-α plays a role in early myocardial remodeling.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Protection from adverse myocardial remodeling secondary to chronic volume overload in mast cell deficient rats

Levick

Gardner

Holland

et al. 2008

Journal of Molecular and Cellular Cardiology

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“…Increased histamine and tryptasc content and mast cell density are also found in the failing heart of patients with idiopathic dilated and ischemic car diomyopathies, two conditions characterised by an increase in fibrous components [101]. Finally, increased mast cell density has been documented in the lesional skin of sclero derma patients [102] and in the lung of patients with bron chial asthma [103] or fibrotic lung disorders [104], Sclero derma patients also showed enhanced basophil releasability compared to that of controls when challenged in vitro with IL-3 and anti-lgE [105], Whether mast cells play a fibrogenic or antifibrogenic role in chronic inflammatory disorders remains to be deter mined.…”

Section: Role Of M a St Cells In Inflam M Atory And Fibrotic D Isordersmentioning

confidence: 99%

Molecular and Cellular Biology of Mast Cells and Basophils

Marone

Casolaro

Patella

et al. 1997

Int Arch Allergy Immunol

113

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In all mammalian species investigated so far, mast cells and basophils are the only cells that synthesize histamine and express plasma membrane receptors that bind IgE with high affinity (FcεRI). Human basophils and mast cells derive from distinct precursors that originate in the bone marrow and fetal liver and probably circulate in peripheral blood. There is extensive evidence that mast cells and basophils and their mediators are primary effectors of allergic inflammation. Immunologically activated human basophils release two cytokines: IL-4 and IL-13. Expression of several cytokines has been documented in a number of experimental models of human and rodent mast cells. However, to date few studies have analyzed the mechanisms of gene expression in human FcεRI+ cells. Some of these studies imply a role for NFAT and GATA family members in the IgE-mediated activation of cytokine gene transcription in basophils and mast cells. Studies of human basophils and mast cells isolated from different anatomic sites have established the different profiles of eicosanoids released by these cells. Recently, the characterization of arachidonic acid pools and the identification of novel enzymes involved in arachidonate remodeling and mobilization clarified in part how eicosanoid productions is regulated in mast cells and basophils. In addition to histamine, human mast cell secretory granules contain the neutral proteases tryptase, chymase and carboxypeptidase that possess several biochemical properties. In particular, tryptase may play a role as a fibrogenic factor and chymase might convert angiotensin I to angiotensin II. Mast cells are present in human heart and in human coronary arteries raising the possibility that local activation of cardiac mast cells might contribute to certain cardiovascular diseases. Recent evidence also suggests that mast cells and basophils can play a role during viral and bacterial infections. It is now evident that in man these two cells not only participate in inflammation associated with allergic disease, but also in chronic and fibrotic disorders affecting several organs and in host defense against bacterial and viral infections.

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“…Mast cells are also known to play roles in cardiovascular pathologies since cardiac mast cell numbers are increased in dilated cardiomyopathy (21) and in the infarct zone post-MI (22). Hara et al (23) further reported that aortic banding in mast cell-deficient mice resulted in reduced perivascular fibrosis in comparison with wild-type mice that had also undergone aortic banding, suggesting a role in hypertension-induced LV fibrosis.…”

Section: Inflammatory Cells and Cardiac Fibrosismentioning

confidence: 99%

Arachidonic Acid Metabolism as a Potential Mediator of Cardiac Fibrosis Associated with Inflammation

Levick

Loch

Taylor

et al. 2007

The Journal of Immunology

101

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An increase in left ventricular collagen (cardiac fibrosis) is a detrimental process that adversely affects heart function. Strong evidence implicates the infiltration of inflammatory cells as a critical part of the process resulting in cardiac fibrosis. Inflammatory cells are capable of releasing arachidonic acid, which may be further metabolized by cyclooxygenase, lipoxygenase, and cytochrome P450 monooxygenase enzymes to biologically active products, including PGs, leukotrienes, epoxyeicosatrienoic acids, and hydroxyeicosatetraenoic acids. Some of these products have profibrotic properties and may represent a pathway by which inflammatory cells initiate and mediate the development of cardiac fibrosis. In this study, we critically review the current literature on the potential link between this pathway and cardiac fibrosis.

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Increased cardiac mast cell density and mediator release in patients with dilated cardiomyopathy

Cited by 43 publications

References 7 publications

Protection from adverse myocardial remodeling secondary to chronic volume overload in mast cell deficient rats

Protection from adverse myocardial remodeling secondary to chronic volume overload in mast cell deficient rats

Molecular and Cellular Biology of Mast Cells and Basophils

Arachidonic Acid Metabolism as a Potential Mediator of Cardiac Fibrosis Associated with Inflammation

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