Mast cell tryptase and chymase in chronic leg ulcers: chymase is potentially destructive to epithelium and is controlled by proteinase inhibitors

Huttunen, Maria; Harvima, Ilkka T.

doi:10.1111/j.1365-2133.2005.06428.x

Cited by 46 publications

(42 citation statements)

References 59 publications

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“…Nevertheless, the increased levels of 1 -AC and 1 -PI within mast cells could well explain the reduced chymase activity. This feature, however, is not speciWc to psoriasis, since it has been detected, for example in basal cell carcinoma [31] as well as chronic leg ulcers [74]. The activation of mast cells in the inXamed skin may lead to granule extrusion and hence loosening of tightly packed acidic granule structure.…”

Section: Mast Cell Serine Proteinases In Psoriasismentioning

confidence: 99%

“…After these observations, several other investigators conWrmed that the number of mast cells is increased in the upper dermis of the psoriatic lesion [59,60,80,189], and it is the MC TC type of mast cells that are increased in number in the uppermost dermis of the psoriatic lesion [61]. However, this change is not speciWc to psoriasis since MC TC mast cells are similarly increased in number in superWcial spreading basal cell carcinoma [31], and mast cells in chronic leg ulcers are predominantly of this MC TC type [74]. Even though mast cells can only rarely be seen in the epidermis of the healthy-looking skin, the presence of mast cells in close association with the epidermis of the psoriatic lesion is a typical feature and sometimes mast cells are present even inside the lesional epidermis [59].…”

Section: Mast Cells In the Psoriatic Lesionmentioning

confidence: 99%

“…In addition, chymase can degrade eotaxin, but not RANTES, MCP-1 or IL-8 [142]. Chymase is a potent enzyme and has to be controlled by proteinase inhibitors since it can aVect the epidermis and cleave epidermal keratinocytes from the substratum leading to keratinocyte apoptosis [74] (Diaconu et al, unpublished results). It can also degrade Wbronectin [138] and activate procollagenase [154].…”

Section: Mast Cell Serine Proteinases In Psoriasismentioning

confidence: 99%

“…Although chymase binds eYciently to heparin, the enzyme remains active also in the absence of heparin, a feature which diVers from that of tryptase. However, heparin can modulate the interaction of chymase with cells, protein substrates and inhibitors [74,159,195]. A clearly distinct feature of chymase is that it can be inactivated by a range of endogenous protease inhibitors, including 1 -proteinase inhibitor ( 1 -PI), 1 -antichymotrypsin ( 1 -AC) [114,161] 2 -macroglobulin [196], secretory leukocyte proteinase inhibitor [195] and squamous cell carcinoma antigen-2 [165].…”

Section: Mast Cell Serine Proteinases In Psoriasismentioning

confidence: 99%

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Is there a role for mast cells in psoriasis?

et al. 2008

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Mast cells have traditionally been considered as eVector cells in allergy but during the last decade it has been realized that mast cells are essentially involved in the mechanisms of innate and acquired immunity. Upon activation by anaphylactic, piecemeal degranulation or degranulation-independent mechanisms mast cells can secrete rapidly or slowly a number of soluble mediators, such as serine proteinases, histamine, lipid-derived mediators, cytokines, chemokines and growth factors. Mast cells can express cell surface co-stimulatory receptors and ligands, and they can express MHC class II molecules and thereby present antigens. These soluble factors and cell surface molecules can interact with other cells, such as endothelial cells, keratinocytes, sensory nerves, neutrophils, T cell subsets and antigen presenting cells which are essential eVectors in the development of skin inXammation. Besides promoting inXammation, mast cells may attempt in some circumstances to suppress the inXammation and epidermal growth but the regulation between suppressive and proinXammatory mechanisms is unclear. Psoriasis is characterized by epidermal hyperplasia and chronic inXammation where tryptase-and chymase-positive MC TC mast cells are activated early in the developing lesion and later the cells increase in number in the upper dermis with concomitant expression of cytokines and TNF superfamily ligands as well as increased contacts with neuropeptide-containing sensory nerves. Due to the intimate involvement of mast cells in immunity and chronic inXammation the role of mast cells in psoriasis is discussed in this review.

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Section: Mast Cell Serine Proteinases In Psoriasismentioning

confidence: 99%

Section: Mast Cells In the Psoriatic Lesionmentioning

confidence: 99%

Section: Mast Cell Serine Proteinases In Psoriasismentioning

confidence: 99%

Section: Mast Cell Serine Proteinases In Psoriasismentioning

confidence: 99%

See 2 more Smart Citations

Is there a role for mast cells in psoriasis?

et al. 2008

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“…Consequently, human tryptase induces vascular tube formation either by direct mitogen action on endothelial cells (18)(19)(20)(21) or by indirect proteolytic action on the surrounding matrix (22)(23)(24). In the latter case, tryptase activates matrix metalloproteinases (MMPs) and plasminogen activator (PA) (25)(26)(27)(28) which, by degrading the extracellular matrix, facilitates an increase of the space available for neovascular growth, while contributing to the release of pro-angiogenic factors, such as VEGF and FGF-2 from the matrix.…”

Section: Introductionmentioning

confidence: 99%

Tryptase serum levels in patients suffering from hepatocellular carcinoma undergoing intra-arterial chemoembolization: Possible predictive role of response to treatment

Goffredo

Gadaleta

Laterza

et al. 2013

Molecular and Clinical Oncology

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Abstract. Tryptase is a serin protease stored in mast cell granules that has recently been found to be involved in tumor angiogenesis. Data from experimental tumor models have suggested that prior to the onset of angiogenesis mast cells were accumulated near tumor cells and were required for the macroscopic expansion and metastatic spread of primary tumor cells. Hepatocellular cancer (HCC) is a well-established, highly angiogenesis-dependent hypervascular tumor. The aim of this preliminary study was to assess tryptase serum levels in 30 HCC patients prior and subsequent to hepatic transarterial chemoembolization (TACE). In this study, patients with intermediate stage (B) HCC, according to the Barcelona Clinic Liver Cancer (BCLC) staging classification, were enrolled. Additional patient features were adequate liver functional reserve and A or B status, according to the Child-Pugh classification. Tryptase levels were measured using the UniCAP-Tryptase fluoroimmunoassay. TACE was performed by loading doxorubicin on microspheres. The mean ± standard deviation (SD) tryptase level pre-TACE was 7.74±3.62 µg/l, and post-TACE 4.67±2.79 µg/l. A statistically significant difference (P<0.001) was detected, using the Student's t-test, between pre-and post-TACE tryptase level concentrations. No correlations were found between tryptase levels and other important clinicopathological features of patients. This is the first preliminary study analyzing the potential significance of serum tryptase levels in HCC patients. The results demonstrated higher serum tryptase levels in HCC patients, suggesting tryptase release from HCC tissue. As expected, after TACE, serum tryptase levels were decreased. Therefore, we suggested that tryptase was a potential biomarker of response to TACE treatment in HCC patients.

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