Mast cells and fibrosis

Atkins, F. M.

doi:10.1001/archderm.123.2.191

Cited by 14 publications

(4 citation statements)

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“…Keloids and hypertrophic scars both contain high numbers of mast cells (Boyadjiev et al , 1995; Hakanson et al , 1969; Harunari et al , 2006; Kischer et al , 1978; Smith et al , 1987), and recently, the mast cell stabilizer ketotifen was shown to reduce contraction and scar tissue deposition in a hypertrophic scar model (Gallant-Behm et al , 2008). Mast cells are also thought to contribute significantly to fibrotic diseases in the skin and other organs, such as scleroderma and pulmonary fibrosis (Atkins and Clark, 1987; Gruber, 2003). Overall, the data presented here provide further evidence that mast cells could be a viable target for anti-fibrosis and anti-scarring therapies.…”

Section: Discussionmentioning

confidence: 99%

Mast Cells Contribute to Scar Formation during Fetal Wound Healing

Wulff

Parent

Meleski

et al. 2012

Journal of Investigative Dermatology

153

129

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Scar formation is a potentially detrimental process of tissue restoration in adults, affecting organ form and function. During fetal development, cutaneous wounds heal without inflammation or scarring at early stages of development, but begin to heal with significant inflammation and scarring as the skin becomes more mature. One possible cell type that could regulate the change from scarless to fibrotic healing is the mast cell. We show here that dermal mast cells in scarless wounds generated at embryonic day 15 (E15) are fewer in number, less mature and do not degranulate in response to wounding as effectively as mast cells of fibrotic wounds made at embryonic day 18 (E18). Differences were also observed between cultured mast cells from E15 and E18 skin with regard to degranulation and preformed cytokine levels. Injection of mast cell lysates into E15 wounds disrupted scarless healing, suggesting that mast cells interfere with scarless repair. Finally, wounds produced at E18, which normally heal with a scar, healed with significantly smaller scars in mast cell-deficient KitW/W-v mice compared to Kit+/+ littermates. Together, these data suggest that mast cells enhance scar formation, and that these cells may mediate the transition from scarless to fibrotic healing during fetal development.

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Section: Discussionmentioning

confidence: 99%

Mast Cells Contribute to Scar Formation during Fetal Wound Healing

Wulff

Parent

Meleski

et al. 2012

Journal of Investigative Dermatology

153

129

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“…Mast cells, which derive from CD34-positive bone marrow stem cells, produce and liberate a variety of biologically active agents, especially monoamines such as histamine. They appear to participate in a variety of inflammatory dermatoses and in some tumors (Atkins and Clark 1987; Melman 1987; Longley et al 1995; Maurer et al 1997; Tada et al 2000). Corresponding to our finding that VMAT2 is present in all cutaneous mast cells of the primate skin, observations in knockout mice lacking the VMAT2 isoform have shown that the quantal release of histamine and serotonin from mast cells is mediated by VMAT2 (Travis et al 2000).…”

Section: Discussionmentioning

confidence: 99%

The Vesicular Monoamine Transporter 2 (VMAT2) Is Expressed by Normal and Tumor Cutaneous Mast Cells and Langerhans Cells of the Skin but Is Absent from Langerhans Cell Histiocytosis

Anlauf

Schäfer

Depboylu

et al. 2004

J Histochem Cytochem.

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S U M M A R YMonoamine storage in secretory granules is mediated by the vesicular monoamine transporters 1 and 2 (VMAT1 and VMAT2). The aim of our study was to identify monoamine-handling normal and neoplastic inflammatory cells in the skin by their expression of VMAT1 and VMAT2. Normal skin from various parts of the body, as well as 21 cases of cutaneous mastocytosis and 10 cases of cutaneous Langerhans cell histiocytosis were analyzed by immunohistochemistry, radioactive in situ hybridization, and doublefluorescence confocal microscopy. VMAT2-positive cells in the subepidermal layer were

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“…MCs have been identified in human liver, and it has been reported that their numbers increase during the course of hepatic diseases associated with excessive extracellular matrix (ECM) deposition (1,2,4,7,15,18,22,23). Increased hepatic MCs have also been observed in a variety of experimental models of rat liver fibrosis (1), including fibrosis induced by porcine serum, radiation, bile duct resection and carbon tetrachloride (CCl 4 ).…”

Section: Introductionmentioning

confidence: 99%

Mast Cell Density, Hepatic Stellate Cell Activation and TGF-β1 Transcripts in the Aging Sprague-Dawley Rat During Early Acute Liver Injury

et al. 2003

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Mast cells (MCs) have been indicated as a source of various inflammatory cytokines, chemokines and growth factors. This study evaluates liver tissue MC density as a quantitative marker of acute liver inflammation in 2-and 19-month old rats treated with carbon tetrachloride (CCl 4 ) to assess the relationships between MC density, hepatocellular damage, mRNA encoding TGF-β 1 , hepatic stellate cell (HSC) activation and collagen levels. Consecutive histological sections from each age group were stained with toluidine blue to identify granulated MCs, Direct Red 80 to recognize collagen matrix, and by immunohistochemistry to identify activated hepatic stellate cells (HSCs), which were subsequently counted by means of a computer-aided image analysis. Histology showed hepatocellular necrosis with inflammatory cell infiltration and collagen matrix deposition. Two and 24 hours after intoxication, MC density had considerably increased in the younger rats, but less in those aged 19 months. Although the untreated older rats had a larger area occupied by activated HSCs than the untreated younger rats, the increase in the number of HSCs was greater in the younger rats both two and 24 hours after intoxication. The greater MC density in younger rats suggests that older rats have a reduced immune response or recruit fewer MCs. The activated HSCs and TGF-β 1 transcripts did not increase significantly during the study period, thus indicating that these are later events in chemically induced hepatic toxicity. In conclusion, MC density may be an index of acute liver inflammation after CCl 4 intoxication.

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Mast cells and fibrosis

Cited by 14 publications

References 0 publications

Mast Cells Contribute to Scar Formation during Fetal Wound Healing

Mast Cells Contribute to Scar Formation during Fetal Wound Healing

The Vesicular Monoamine Transporter 2 (VMAT2) Is Expressed by Normal and Tumor Cutaneous Mast Cells and Langerhans Cells of the Skin but Is Absent from Langerhans Cell Histiocytosis

Mast Cell Density, Hepatic Stellate Cell Activation and TGF-β1 Transcripts in the Aging Sprague-Dawley Rat During Early Acute Liver Injury

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