scholarly journals The Mast Cell–SCF–CB1 Interaction Is a Key Player in Seborrheic Keratosis

2020 ◽  
Vol 68 (7) ◽  
pp. 461-471
Author(s):  
Mika Yamanaka-Takaichi ◽  
Koji Sugawara ◽  
Rieko Sumitomo ◽  
Daisuke Tsuruta
Keyword(s):  
Atopic Dermatitis ◽  
Mast Cell ◽  
Stem Cell ◽  
Stem Cell Factor ◽  
Skin Diseases ◽  
Cannabinoid Receptor ◽  
Seborrheic Keratosis ◽  
Novel Treatment ◽  
Important Player

Mast cell (MC) is an important player in the development of skin diseases, including atopic dermatitis, psoriasis, and urticaria. It is reported that MC infiltration and activation are observed around various types of tumors and speculated that MCs play key roles in their pathogenesis. As MCs in human seborrheic keratosis (SK) have not been well investigated, here we focused on the MCs in SK. The number of c-Kit and tryptase-positive MCs was significantly increased around the SK compared with the marginal lesion. Degranulated MCs were also increased around the tumors. Furthermore, MC growth factor, stem cell factor (SCF), expression within the SK was significantly upregulated compared with the marginal lesion. Interestingly, one of the cognitive regulators of SCF expression, cannabinoid receptor type 1 (CB1) immunoreactivity was downregulated within the SK. Our results suggest that MCs play important roles in the pathogenesis of SK and that SCF can be also deeply involved in the development of SKs. Our current results highlight the CB1–SCF–MC interaction as a novel mechanism of SK development and this also will be utilized for developing a novel treatment.

scholarly journals SHP2 Phosphatase Promotes Mast Cell Chemotaxis toward Stem Cell Factor via Enhancing Activation of the Lyn/Vav/Rac Signaling Axis

2014 ◽  
Vol 192 (10) ◽  
pp. 4859-4866 ◽  
Author(s):  
Namit Sharma ◽  
Stephanie Everingham ◽  
Baskar Ramdas ◽  
Reuben Kapur ◽  
Andrew W. B. Craig
Keyword(s):  
Mast Cell ◽  
Stem Cell ◽  
Stem Cell Factor ◽  
Signaling Axis ◽  
Cell Chemotaxis

Βeta-eudesmol reduces stem cell factor-induced mast cell migration

2017 ◽  
Vol 48 ◽  
pp. 1-7 ◽  
Author(s):  
Sun-Young Nam ◽  
Hee-Yun Kim ◽  
Hyung-Min Kim ◽  
Hyun-Ja Jeong
Keyword(s):  
Mast Cell ◽  
Stem Cell ◽  
Cell Migration ◽  
Stem Cell Factor

scholarly journals The rat c-kit ligand, stem cell factor, induces c-kit receptor-dependent mouse mast cell activation in vivo. Evidence that signaling through the c-kit receptor can induce expression of cellular function.

1992 ◽  
Vol 175 (1) ◽  
pp. 245-255 ◽  
Author(s):  
B K Wershil ◽  
M Tsai ◽  
E N Geissler ◽  
K M Zsebo ◽  
S J Galli
Keyword(s):  
Mast Cell ◽  
Stem Cell ◽  
Mast Cells ◽  
Stem Cell Factor ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Tyrosine Kinase Receptor ◽  
Kit Ligand ◽  
Kit Receptor

Interactions between products of the mouse W locus, which encodes the c-kit tyrosine kinase receptor, and the Sl locus, which encodes a ligand for c-kit receptor, which we have designated stem cell factor (SCF), have a critical role in the development of mast cells. Mice homozygous for mutations at either locus exhibit several phenotypic abnormalities including a virtual absence of mast cells. Moreover, the c-kit ligand SCF can induce the proliferation and maturation of normal mast cells in vitro or in vivo, and also can result in repair of the mast cell deficiency of Sl/Sld mice in vivo. We now report that administration of SCF intradermally in vivo results in dermal mast cell activation and a mast cell-dependent acute inflammatory response. This effect is c-kit receptor dependent, in that it is not observed when SCF is administered to mice containing dermal mast cells expressing functionally inactive c-kit receptors, is observed with both glycosylated and nonglycosylated forms of SCF, and occurs at doses of SCF at least 10-fold lower on a molar basis than the minimally effective dose of the classical dermal mast cell-activating agent substance P. These findings represent the first demonstration in vivo that a c-kit ligand can result in the functional activation of any cellular lineage expressing the c-kit receptor, and suggest that interactions between the c-kit receptor and its ligand may influence mast cell biology through complex effects on proliferation, maturation, and function.

scholarly journals Cofactors are essential for stem cell factor-dependent growth and maturation of mast cell progenitors: comparative effects of interleukin- 3 (IL-3), IL-4, IL-10, and fibroblasts

Blood ◽  
1995 ◽  
Vol 85 (1) ◽  
pp. 57-65 ◽  
Author(s):  
D Rennick ◽  
B Hunte ◽  
G Holland ◽  
L Thompson-Snipes
Keyword(s):  
Mast Cell ◽  
Stem Cell ◽  
Cell Differentiation ◽  
Mast Cells ◽  
Colony Formation ◽  
Stem Cell Factor ◽  
Interleukin 10 ◽  
Interleukin 4 ◽  
Phenotypic Change ◽  
Interleukin 3

Stem cell factor (SCF) possesses many mast cell-stimulating activities, including the ability to support the growth of mucosal-like mast cells (MMCs) and connective tissue mast cells (CTMCs). However, this study shows that, in the absence of accessory cells, SCF does not stimulate the clonal growth of primitive mast cell progenitors. Nevertheless, SCF exhibited potent growth-promoting effects when combined with the cytokines interleukin-3 (IL-3), interleukin-4 (IL-4), and interleukin- 10 (IL-10). Our comparative studies have shown that optimal mast cell colony formation occurs when both IL-4 and IL-10 are combined with SCF. However, in the presence of SCF, these two cofactors appear to mediate different effects. IL-4 was more efficient than IL-10 in costimulating the initiation of SCF-dependent colony formation by mast cell progenitors and in sustaining the proliferation of newly generated progeny. On the other hand, IL-4 was less efficient than IL-10 in supporting mast cell differentiation, as evidenced by morphology, cell enlargement, and granule production. Although the actions of IL-4 and IL-10 were not equivalent, additional experiments indicated that their ability to serve as early- and late-acting factors, respectively, were complimentary. We have also found that the mast cells generated in colonies stimulated by IL-4, IL-10, and SCF produced high levels of histamine (6–8 pg per cell). None of the mast cells generated in our cultures synthesized heparin. A phenotypic change from safranin- negative to safranin-positive cells associated with heparin-producing CTMCs was accomplished after coculture of the mast cells with fibroblast cell lines derived from normal mice or from SI/SId mice plus soluble factors. Collectively, our observations demonstrate that SCF acts as a competence factor for mast cell progenitor growth. In addition, the ability of SCF to support certain stages of mast cell differentiation is profoundly influenced by interactions with specific cofactors.

Eotaxin Modulates Myelopoiesis and Mast Cell Development From Embryonic Hematopoietic Progenitors

Blood ◽  
1998 ◽  
Vol 92 (6) ◽  
pp. 1887-1897 ◽  
Author(s):  
Elizabeth J. Quackenbush ◽  
Barry K. Wershil ◽  
Vincent Aguirre ◽  
Jose-Carlos Gutierrez-Ramos
Keyword(s):  
Mast Cell ◽  
Stem Cell ◽  
Mast Cells ◽  
Stem Cell Factor ◽  
Fetal Liver ◽  
Hematopoietic Progenitors ◽  
Embryonic Tissues ◽  
Pathological Conditions ◽  
Gi Protein ◽  
American Society

Abstract Eotaxin is a potent chemoattractant for eosinophils during inflammation and allergic reactions in the adult, but its role in the embryonic development of the hematopoietic system has not been examined. We report here that eotaxin and its receptor, CCR-3, are expressed by embryonic tissues responsible for blood development, such as fetal liver (FL), yolk sac (YS), and peripheral blood. We found that eotaxin acts synergistically with stem cell factor to accelerate the differentiation of embryonic mast cell progenitors, and this response can be suppressed by pertussis toxin, an inhibitor of chemokine-induced signaling through Gi protein and chemotaxis. Eotaxin promotes the differentiation of fetal mast cell progenitors into differentiated mast cells as defined by the expression of mast cell specific proteases. Furthermore, in combination with stem cell factor (SCF), it promotes the growth of Mac-1+myeloid cells from embryonic progenitors. These studies suggest that eotaxin may be involved in the growth of granulocytic progenitors and the differentiation and/or function of mast cells during embryogenesis and/or pathological conditions that induce high levels of eotaxin, such as allergic responses. © 1998 by The American Society of Hematology.

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