Human mast cells produce matrix metalloproteinase 9

Kanbe, Naotomo; Tanaka, Akane; Kanbe, Michiyo; Itakura, Atsuko; Kurosawa, Motohiro; Matsuda, Hiroshi

doi:10.1002/(sici)1521-4141(199908)29:08<2645::aid-immu2645>3.0.co;2-1

Cited by 112 publications

(54 citation statements)

References 15 publications

(12 reference statements)

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“…A similar pattern of regulation of MMP-9 by TNF-␣ and IFN-␥ has previously been reported in human macrophages (47), however its regulation by TNF-␣ and IFN-␥ in primary human mast cells (CB-HMC) is novel. Although the production of MMP-9 by human mast cells has been reported (23,(33)(34)(35)(36)(37)44), we provide substantial evidence to demonstrate that MMP-9 is primarily not a stored product. Other investigators have speculated that latent MMP-9 coexists with histamine and tryptase in specialized secretory granules within mast cells (37).…”

Section: Discussionmentioning

confidence: 53%

“…In addition to the well-characterized serine proteases, previous studies have identified members of the MMPs in these cells (22,(33)(34)(35)(36)(37)44). Initially, it was our intention to confirm these primarily in vitro observations in vivo, using synovial tissue obtained from patients with RA by immunohistochemistry.…”

Section: Production Of Mmp-9 By Human Mast Cells In Vivomentioning

confidence: 97%

“…Relevant to acute and chronic inflammation, MMP-9 can cleave IL-8 and potentiate its activity as a neutrophil chemoattractant by at least 10-fold (18). There is now compelling evidence that along with the arsenal of stored serine proteases, mast cells are also a major source of MMPs such as MMP-1 (33), , and MMP-9 (23,(35)(36)(37). Although there is limited evidence for the expression of MMP-9 in mast cells in rheumatoid synovium (35), its regulation in RA is poorly understood.…”

Section: Ast Cells Are Derived From Hemopoietic Progenitor Cells Thmentioning

confidence: 99%

“…There is now compelling evidence that along with the arsenal of stored serine proteases, mast cells are also a major source of MMPs such as MMP-1 (33), , and MMP-9 (23,(35)(36)(37). Although there is limited evidence for the expression of MMP-9 in mast cells in rheumatoid synovium (35), its regulation in RA is poorly understood. In the current study, we confirm MMP-9 expression in rheumatoid synovial mast cells and for the first time, demonstrate its regulation by TNF-␣ and IFN-␥ in cord blood-derived human mast cells (CB-HMC), bone marrow-derived mouse mast cells (mBMMC), and the human mast cell line-1 (HMC-1).…”

Section: Ast Cells Are Derived From Hemopoietic Progenitor Cells Thmentioning

confidence: 99%

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Human Mast Cell-Derived Gelatinase B (Matrix Metalloproteinase-9) Is Regulated by Inflammatory Cytokines: Role in Cell Migration

Girolamo

Indoh

Jackson

et al. 2006

The Journal of Immunology

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Mast cells are key effectors in the pathogenesis of inflammatory and tissue destructive diseases such as rheumatoid arthritis (RA). These cells contain specialized secretory granules loaded with bioactive molecules including cytokines, growth factors, and proteases that are released upon activation. This study investigated the regulation of matrix metalloproteinase MMP-9 (gelatinase B) in human mast cells by cytokines that are known to be involved in the pathogenesis of RA. Immunohistochemical staining of synovial tissue showed abundant expression of MMP-9 by synovial tissue mast cells in patients with RA but not in normal controls. The expression, activity, and production of MMP-9 in mast cells was confirmed by RT-PCR, zymography, and Western blotting using cord blood-derived human mast cells (CB-HMC). Treatment of CB-HMC with TNF-α significantly increased the expression of MMP-9 mRNA and up-regulated the activity of MMP-9 in a time- and dose-dependent manner. By contrast, IFN-γ inhibited MMP-9 mRNA and protein expression. The cytokine-mediated regulation of MMP-9 was also apparent in the human mast cell line (HMC-1) and in mouse bone marrow-derived mast cells. Furthermore, TNF-α significantly increased the invasiveness of CB-HMC across Matrigel-coated membranes while the addition of IFN-γ, rTIMP-1, or pharmacological MMP inhibitors significantly reduced this process. These observations suggest that MMP-9 is not a stored product in mast cells but these cells are capable of producing this enzyme under inflammatory conditions that may facilitate the migration of mast cell progenitors to sites of inflammation and may also contribute to local tissue damage.

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Section: Discussionmentioning

confidence: 53%

Section: Production Of Mmp-9 By Human Mast Cells In Vivomentioning

confidence: 97%

Section: Ast Cells Are Derived From Hemopoietic Progenitor Cells Thmentioning

confidence: 99%

Section: Ast Cells Are Derived From Hemopoietic Progenitor Cells Thmentioning

confidence: 99%

See 2 more Smart Citations

Human Mast Cell-Derived Gelatinase B (Matrix Metalloproteinase-9) Is Regulated by Inflammatory Cytokines: Role in Cell Migration

Girolamo

Indoh

Jackson

et al. 2006

The Journal of Immunology

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“…It was also reported that ATP induces the release of matrix metalloproteinase-9 via a P2X 7 -dependent mechanism [95]. Mast cells are a rich source of this enzyme that participates in extracellular matrix remodeling by catalyzing the degradation of type IV collagen, the main component of the basement membrane [96].…”

Section: Purinergic Signaling In Allergic Airway Inflammation: Focus mentioning

confidence: 99%

P2 receptor-mediated signaling in mast cell biology

Bulanova

Bulfone–Paus∥

2009

Purinergic Signalling

101

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Mast cells are widely recognized as effector cells of allergic inflammatory reactions. They contribute to the pathogenesis of different chronic inflammatory diseases, wound healing, fibrosis, thrombosis/fibrinolysis, and antitumor immune responses. In this paper, we summarized the role of P2X and P2Y receptors in mast cell activation and effector functions. Mast cells are an abundant source of ATP which is stored in their granules and secreted upon activation. We discuss the contribution of mast cells to the extracellular ATP release and to the maintenance of extracellular nucleotides pool. Recent publications highlight the importance of purinergic signaling for the pathogenesis of chronic airway inflammation. Therefore, the role of ATP and P2 receptors in allergic inflammation with focus on mast cells was analyzed. Finally, ATP functions as mast cell autocrine/paracrine factor and as messenger in intercellular communication between mast cells, nerves, and glia in the central nervous system.

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c‐Kit immunophenotyping and metalloproteinase expression profiles of mast cells in interstitial lung diseases

Edwards

Cruz

Donnelly

et al. 2005

The Journal of Pathology

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Diverse interstitial lung diseases (ILD) demonstrate mesenchymal infiltration by an abundance of activated mast cells whose role in parenchymal fibrogenesis remains unclear. Since mast cells differentiate in a dynamic, tissue-specific manner via signals transduced by c-Kit receptor, we examined the effect of ILD microenvironments on c-Kit expression and metalloproteinase phenotypes of mesenchymal mast cell populations. Immunohistochemical and flow cytometric analyses characterized surface expression of c-Kit on mast cells in tissues obtained from patients with idiopathic pulmonary fibrosis, systemic sclerosis, sarcoidosis, and lymphangioleiomyomatosis, thus identifying a unique immunophenotype not shared by normal lung mast cells. Isolation of c-Kit+/FcepsilonRI+/CD34- mast cells via immunocytometric sorting of heterogeneous cell populations from mechanically disaggregated lung tissues permitted analysis of gene expression patterns by two-step real-time polymerase chain reaction. Transcriptional profiling identified expression of c-Kit and the neutral serine proteases, tryptase and chymase, establishing the identity of sorted populations as mature mast cells. Mast cells harvested from ILD tissues demonstrated characteristic metalloproteinase phenotypes which included expression of matrix metalloproteinase (MMP)-1 and a disintegrin and metalloproteinase (ADAM)-9, -10, and -17. Immunohistochemical co-localization guided by gene profiling data confirmed expression of chymase, MMP-1, and ADAM-17 protein in subpopulations of mast cells in remodelling interstitium. Gene profiling of harvested mast cells also showed increased transcript copy numbers for TNFalpha and CC chemokine receptor 2, which play critical roles in lung injury. We conclude that ILD microenvironments induce unique c-Kit receptor and metalloproteinase mast cell phenotypes.

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Human mast cells produce matrix metalloproteinase 9

Cited by 112 publications

References 15 publications

Human Mast Cell-Derived Gelatinase B (Matrix Metalloproteinase-9) Is Regulated by Inflammatory Cytokines: Role in Cell Migration

Human Mast Cell-Derived Gelatinase B (Matrix Metalloproteinase-9) Is Regulated by Inflammatory Cytokines: Role in Cell Migration

P2 receptor-mediated signaling in mast cell biology

c‐Kit immunophenotyping and metalloproteinase expression profiles of mast cells in interstitial lung diseases

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