Mast Cell-Fibroblast Interactions Induce Matrix Metalloproteinase-9 Release from Fibroblasts: Role for IgE-Mediated Mast Cell Activation

Abel, M; Vliagoftis, Harissios

doi:10.4049/jimmunol.180.5.3543

Cited by 41 publications

(26 citation statements)

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“…The increase in MMP14, however, was only partially suppressed (by 45%) with apocynin. These TNF-mediated changes in MMP expressions were 1 The online version of this article contains supplemental material. well reflected in the proteolytic activities of these culture systems.…”

Section: Tnf-induced Superoxide Production Is Accelerated and Strongementioning

confidence: 97%

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Tumor necrosis factor induces matrix metalloproteinases in cardiomyocytes and cardiofibroblasts differentially via superoxide production in a PI3Kγ-dependent manner

Awad

Kandalam

Chakrabarti

et al. 2010

American Journal of Physiology-Cell Physiology

106

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Tumor necrosis factor (TNF) is an inflammatory cytokine that is upregulated in a number of cardiomyopathies. Adverse cardiac remodeling and dilation result from degradation of the extracellular matrix by matrix metalloproteinases (MMPs). We investigated whether TNF can directly trigger expression and activation of MMPs in cardiac cells. We compared MMP expression profile and activities between primary cultures of mouse neonatal cardiomyocytes and cardiofibroblasts and in cellular and extracellular compartments. In response to recombinant TNF (rTNF, 20 ng/ml), cardiomyocytes exhibited faster and more pronounced superoxide production compared with cardiofibroblasts, concomitant with increased expression of several MMPs. MMP9 levels increased more rapidly and about twofold more in cardiomyocytes than in cardiofibroblasts. TNF did not induce MMP2 expression. Expression of collagenases (MMP8, MMP12, MMP13, and MMP14) increased significantly, while total collagenase activity increased to a greater degree in conditioned medium of cardiomyocytes than in cardiofibroblasts. rTNF-mediated MMP expression and activation were dependent on superoxide production and were blocked by apocynin, an NADPH oxidase inhibitor. We identified phosphatidylinositol 3-kinase (PI3K)gamma as a key factor in TNF-mediated events since TNF-induced superoxide production, MMP expression, and activity were significantly suppressed in cardiomyocytes and cardiofibroblasts deficient in PI3Kgamma. We further demonstrated that the TNF-superoxide-MMP axis of events is in fact activated in heart disease in vivo. Wild-type and TNF(-/-) mice subjected to cardiac pressure overload revealed that TNF deficiency resulted in reduced superoxide levels, collagenase activities, PI3K activity, and fibrosis leading to attenuated cardiac dilation and dysfunction. Our study demonstrates that TNF triggers expression and activation of MMPs faster and stronger in cardiomyocytes than in cardiofibroblasts in a superoxide-dependent manner and via activation of PI3Kgamma, thereby contributing to adverse myocardial remodeling in disease.

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Section: Tnf-induced Superoxide Production Is Accelerated and Strongementioning

confidence: 97%

“…S1A). 1 Concomitantly, a rise in nitrate/nitrite (NO 2 /NO 3 ) levels was also detected as measured by Griess reaction assay (Fig. 2B), suggestive of enhanced activity of NOS and elevated NO production.…”

Section: Tnf-induced Superoxide Production Is Accelerated and Strongementioning

confidence: 98%

Tumor necrosis factor induces matrix metalloproteinases in cardiomyocytes and cardiofibroblasts differentially via superoxide production in a PI3Kγ-dependent manner

Awad

Kandalam

Chakrabarti

et al. 2010

American Journal of Physiology-Cell Physiology

106

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“…Mouse bone marrow-derived mast cells (BMMCs) were generated from 6-week-old C57BL/6 mice according to the method described previously [15]. Briefly, bone marrow cells in alpha modification of Eagle's medium (α-MEM; Invitrogen, Carlsbad, Calif., USA) containing 10% FBS, 100 U/ml penicillin G, 100 μg/ml streptomycin, 1 m M sodium pyruvate, 0.1 m M nonessential amino acid, and 50 μ M 2-mercaptoethanol (Invitrogen) supplemented with 10 ng/ml mIL-3 (PeproTech, Rocky Hill, N.J., USA) were cultured at 37°C in a humidified atmosphere of 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

Inhibition of MMP-2-Mediated Mast Cell Invasion by NF-κB Inhibitor DHMEQ in Mast Cells

Noma¹,

Asagiri²,

Takeiri³

et al. 2015

Int Arch Allergy Immunol

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Background: Stimulation with antigen and IgE is known to activate NF-κB in mast cells. In the present research, we studied the role of NF-κB on cellular migration in mast cell-like RBL-2H3 cells and bone marrow-derived mast cells (BMMCs) using the NF-κB inhibitor (-)-DHMEQ. Methods: A Matrigel invasion chamber was used to evaluate cell migration. A PCR array was used to screen the expression of 84 key genes involved in cell migration. Results: (-)-DHMEQ inhibited antigen/IgE-induced NF-κB activation and expressions of its target genes such as IL-6 and TNF-α. (-)-DHMEQ was found to inhibit in vitro invasion toward the antigen without any toxicity. We then looked for NF-κB-dependent genes that would be important for mast cell invasion using the PCR array. (-)-DHMEQ was found to lower the expression of matrix metalloproteinase (MMP)-2. The MMP inhibitor GM6001 also inhibited cellular invasion toward the antigen. These effects of (-)-DHMEQ were obtained in both RBL-2H3 cells and BMMCs. Conclusions: These findings indicate that (-)-DHMEQ suppressed mast cell migration via the inhibition of NF-κB-regulated MMP-2 expression.

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“…In this study, mast cells were found in close contact with fibroblasts. Mast cell activation is a characteristic feature of chronic inflammation, a condition that may lead to fibrosis as a result of increased collagen synthesis by a fibroblast [140][141][142][143][144].…”

Section: Cell-cell Interaction In Dermal Resident Cellsmentioning

confidence: 99%

“…Fibroblasts can modulate the functions of both mast cells and eosinophils, which also increase the amount of melanocytes and melanin pigment [141][142][143].…”

Section: Cell-cell Interaction In Dermal Resident Cellsmentioning

confidence: 99%

Cell-Cell Interactions and Cross Talk Described in Normal and Disease Conditions: Morphological Approach

Ayuob¹,

Ali²

2012

Cell Interaction

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Additional information is available at the end of the chapter http://dx.doi.org/10.5772/48435 IntroductionThe contact between cells and their microenvironment is fundamental both during development and for the preservation of tissue structure. Picking out the signals coming from the surrounding environment enable cells to react promptly to changes that may occur. Various molecular mechanisms explain the ability of cells to sense the microenvironment could be grouped into two major classes: (1) the transmission of signals in the form of soluble molecules which interact with cellular receptors, such as growth factors, cytokines, hormones, etc., and (2) the interaction of cells with structural components of their environment, namely other cells and the extracellular matrix (ECM) [1].Cell-cell interactions are central to the function of many organ systems. A common theme for heterotypic cell interactions is the interaction of parenchymal cells with nonparenchymal neighbors with resultant modulation of cell growth, migration, and/or differentiation. Specifically, these interactions are of fundamental importance in physiology [2,3], pathophysiology [4,5], cancer [6,7] developmental biology [8,9], wound healing [10,11], and attempts to replace tissue function through 'tissueengineering' [12,13]. Further understanding of how cell-cell interactions modulate tissue function will allow us to gain fundamental biological insight as well as suggest approaches that will allow the manipulation of tissue function in vitro for therapeutic applications in vitro for therapeutic applications [14]. Cell-cell interaction and cross talk phenomena during embryonic periodCells are the true miracle of evolution. Once the basic building block, the eukaryotic cell, became available, the form of metazoans evolved by changing the arrangement of cells with respect to each other. Cell-cell interaction in embryo was described in literature to have a

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Mast Cell-Fibroblast Interactions Induce Matrix Metalloproteinase-9 Release from Fibroblasts: Role for IgE-Mediated Mast Cell Activation

Cited by 41 publications

References 50 publications

Tumor necrosis factor induces matrix metalloproteinases in cardiomyocytes and cardiofibroblasts differentially via superoxide production in a PI3Kγ-dependent manner

Tumor necrosis factor induces matrix metalloproteinases in cardiomyocytes and cardiofibroblasts differentially via superoxide production in a PI3Kγ-dependent manner

Inhibition of MMP-2-Mediated Mast Cell Invasion by NF-κB Inhibitor DHMEQ in Mast Cells

Cell-Cell Interactions and Cross Talk Described in Normal and Disease Conditions: Morphological Approach

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