scholarly journals DIFFERENTIATION AND PROLIFERATION OF EMBRYONIC MAST CELLS OF THE RAT

1965 ◽  
Vol 25 (3) ◽  
pp. 577-592 ◽  
Author(s):  
J. W. Combs ◽  
D. Lagunoff ◽  
E. P. Benditt
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Alcian Blue ◽  
Stage Iv ◽  
Cytoplasmic Granules ◽  
Morphologic Characteristics ◽  
Proliferation And Differentiation ◽  
Mitotic Figures ◽  
Differentiation And Proliferation ◽  
Mast Cell Chymase

Histochemical reactions and radioautography were used to investigate the sequence of mast cell development in rat embryos. Mast cells arise ubiquitously in and are confined to the loose connective tissue in the embryo. The alcian blue-safranin reaction distinguishes between weakly sulfated and strongly sulfated mucopolysaccharides by a shift from alcian blue to safranin staining. Based on this reaction and morphologic characteristics, four stages were identified. Stage I mast cells are lymphocyte-like cells with cytoplasmic granules which invariably stain blue with the alcian blue-safranin reaction. In Stage II cells the majority of granules are alcian blue-positive, but some safranin-positive granules have appeared. Stage III mast cells are distinguished by a majority of safranin-positive cytoplasmic granules; some alcian blue-positive granules still remain. Stage IV cells contain only safranin-positive granules. Thymidine-H3 uptake and identification of mitotic figures indicates that mast cells in Stages I and II comprise a mitotic pool while those in Stages III and IV are mitotically inactive. The pattern of S35O4 incorporation and the sequence of appearance of histochemically identifiable mast cell constituents corroborates division of the proliferation and differentiation of embryonic mast cells into the four stages described above. The process of formation of mast cell granules is interpreted as reflecting the synthesis and accumulation of a heparin precursor in alcian blue positive granules followed by the synthesis and accumulation of highly N-sulfated heparin along with mast cell chymase and finally histamine in safranin-positive granules.

scholarly journals Mast Cell Chymase and Kidney Disease

2020 ◽  
Vol 22 (1) ◽  
pp. 302
Author(s):  
Shamila Vibhushan ◽  
Manuela Bratti ◽  
Juan Eduardo Montero-Hernández ◽  
Alaa El Ghoneimi ◽  
Marc Benhamou ◽  
...  
Keyword(s):  
Mast Cell ◽  
Angiotensin Ii ◽  
Mast Cells ◽  
Kidney Disease ◽  
Inflammatory Response ◽  
Inflammatory Mediator ◽  
Total Proteins ◽  
Cytoplasmic Granules ◽  
Physiological Processes ◽  
Mast Cell Chymase

A sizable part (~2%) of the human genome encodes for proteases. They are involved in many physiological processes, such as development, reproduction and inflammation, but also play a role in pathology. Mast cells (MC) contain a variety of MC specific proteases, the expression of which may differ between various MC subtypes. Amongst these proteases, chymase represents up to 25% of the total proteins in the MC and is released from cytoplasmic granules upon activation. Once secreted, it cleaves the targets in the local tissue environment, but may also act in lymph nodes infiltrated by MC, or systemically, when reaching the circulation during an inflammatory response. MC have been recognized as important components in the development of kidney disease. Based on this observation, MC chymase has gained interest following the discovery that it contributes to the angiotensin-converting enzyme’s independent generation of angiotensin II, an important inflammatory mediator in the development of kidney disease. Hence, progress regarding its role has been made based on studies using inhibitors but also on mice deficient in MC protease 4 (mMCP-4), the functional murine counterpart of human chymase. In this review, we discuss the role and actions of chymase in kidney disease. While initially believed to contribute to pathogenesis, the accumulated data favor a more subtle view, indicating that chymase may also have beneficial actions.

Mast Cell Heterogeneity in Human Lung Tissue

1989 ◽  
Vol 77 (3) ◽  
pp. 297-304 ◽  
Author(s):  
F. J. Van Overveld ◽  
L. A. M. J. Houben ◽  
F. E. M. Schmitz du Moulin ◽  
P. L. B. Bruijnzeel ◽  
J. A. M. Raaijmakers ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Alcian Blue ◽  
Lung Tissue ◽  
Human Lung ◽  
Immunoglobulin E ◽  
Prostaglandin D2 ◽  
Leukotriene C4 ◽  
Human Lung Tissue ◽  
No Release

1. In this study mast cells were found to comprise 2.1% of total cells recovered by enzymatic digestion of human lung tissue. 2. This mast cell population consisted of 79% formalin-sensitive, Alcian Blue-positive mast cells and 21% formalin-insensitive, Alcian Blue-positive mast cells. 3. By the use of centrifugal elutriation and subsequent Percoll gradient centrifugation, separate mixed cell populations could be obtained in which the mast cell constituents were either of the formalin-sensitive or -insensitive type. 4. Cell suspensions in which formalin-sensitive cells comprised 97% of mast cells contained approximately 1.34 pg of histamine per mast cell, whereas in preparations in which mast cells were 84% formalin-resistant the histamine content was approximately 4.17 pg of histamine per mast cell. 5. The histamine release upon anti-immunoglobulin E challenge of formalin-sensitive mast cells was greater than the release by formalin-insensitive mast cells. 6. After challenge with opsonized zymosan, only formalin-sensitive mast cells were able to release histamine. 7. Leukotriene C4 release was observed when formalin-sensitive mast cells were challenged with antiimmunoglobulin E. Formalin-insensitive mast cells showed no release of leukotriene C4. 8. Prostaglandin D2 release was observed when formalin-insensitive mast cells were challenged with antiimmunoglobulin E. Formalin-sensitive mast cells showed no release of prostaglandin D2.

Role of endothelin-converting enzyme, chymase and neutral endopeptidase in the processing of big ET-1, ET-1(1-21) and ET-1(1-31) in the trachea of allergic mice

2002 ◽  
Vol 103 (s2002) ◽  
pp. 353S-356S ◽  
Author(s):  
Benjamin A. DE CAMPO ◽  
Roy G. GOLDIE ◽  
Arco Y. JENG ◽  
Peter J. HENRY
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Response Curve ◽  
Histological Analysis ◽  
Neutral Endopeptidase ◽  
Converting Enzyme ◽  
Rightward Shift ◽  
Endothelin Converting Enzyme ◽  
Mast Cell Chymase

The present study examined the roles of endothelin-converting enzyme (ECE), neutral endopeptidase (NEP) and mast cell chymase as processors of the endothelin (ET) analogues ET-1(1–21), ET-1(1–31) and big ET-1 in the trachea of allergic mice. Male CBA/CaH mice were sensitized with ovalbumin (10µg) delivered intraperitoneal on days 1 and 14, and exposed to aerosolized ovalbumin on days 14, 25, 26 and 27 (OVA mice). Mice were killed and the trachea excised for histological analysis and contraction studies on day 28. Tracheae from OVA mice had 40% more mast cells than vehicle-sensitized mice (sham mice). Ovalbumin (10µg/ml) induced transient contractions (15±3% of the Cmax) in tracheae from OVA mice. The ECE inhibitor CGS35066 (10µM) inhibited contractions induced by big ET-1 (4.8-fold rightward shift of dose-response curve; P<0.05), but not those induced by either ET-1(1–21) or ET-1(1–31). The chymase inhibitors chymostatin (10µM) and Bowman-Birk inhibitor (10µM) had no effect on contractions induced by any of the ET analogues used. The NEP inhibitor CGS24592 (10µM) inhibited contractions induced by ET-1(1–31) (6.2-fold rightward shift; P<0.05) but not ET-1(1–21) or big ET-1. These data suggest that big ET-1 is processed predominantly by a CGS35066-sensitive ECE within allergic airways rather than by mast cell-derived proteases such as chymase. If endogenous ET-1(1–31) is formed within allergic airways, it is likely to undergo further conversion by NEP to more active products.

scholarly journals Abnormal mast cell granules in the beige (Chédiak-Higashi syndrome) mouse.

1975 ◽  
Vol 23 (2) ◽  
pp. 117-122 ◽  
Author(s):  
E Y Chi ◽  
D Lagunoff
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Alcian Blue ◽  
Toluidine Blue ◽  
Ruthenium Red ◽  
Chediak Higashi Syndrome

Mast cells of beige (C57BL/6J) (bg-j/bg-j) mice were examined histochemically and ultrastructurally. Mast cell granules in the beige mice were markedly enlarged and irregular in shape. Granule contents stained uniformly with acidified toluidine blue, but with ruthenium red and Alcian Blue-safranin, two components were evident. The rims of the abnormal granules stained with ruthenium red and with Alcian Blue; the centers of the granules were clear with ruthenium red and stained with safranin. Mast cell granules thus represent another abnormal organelle in the Chédiak-Higashi syndrome.

scholarly journals The presence of mast cell precursors in rat peripheral blood

Blood ◽  
1981 ◽  
Vol 58 (3) ◽  
pp. 544-551 ◽  
Author(s):  
D Zucker-Franklin ◽  
G Grusky ◽  
N Hirayama ◽  
E Schnipper
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Alcian Blue ◽  
Peripheral Blood ◽  
Periodic Acid ◽  
Phenotypic Expression ◽  
Soft Agar ◽  
Sulfated Polysaccharides ◽  
Periodic Acid Schiff ◽  
Agar Culture

Abstract Soft agar culture of mononuclear cell fractions prepared from rat peripheral blood yielded numerous colonies consisting of mast cells. The mast cell nature of the cells was established by ultrastructural and histochemical analyses as well as by the demonstration the the colonies contained histamine and that the cells possessed receptors for the Fc component of IgE. Stringent criteria for the distinction of mast cells from monocytes/macrophages that could have metachromatic inclusions were applied. The alcian-blue-safranin technique delineated the maturation of mast cell granules by showing the loss of alcian-blue and increase in safranin-positive organelles presumed to reflect the increase in N-sulfated polysaccharides representing heparin. The mast cells exhibited low or absent reactions for peroxidase, alpha-naphthyl butyrate, periodic acid Schiff, and Sudan black reacting lipid, whereas macrophages stained in parallel were positive for these substances. Since it is known that extracellular conditions may cause variations in phenotypic expression, the observations have led to the hypothesis that mast cells and macrophages may have a common precursor.

An improved method for staining mouse mast cells

1989 ◽  
Vol 67 (1) ◽  
pp. 226-227 ◽  
Author(s):  
M. Novak ◽  
S. Nombrado
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Connective Tissue ◽  
Alcian Blue ◽  
Cell Types ◽  
Mucosal Mast Cell ◽  
Improved Method ◽  
Tissue Mast Cell ◽  
Pathological Conditions

An improved method for staining mouse mast cells with alcian blue is reported. The reaction differentiates between mucosal mast cell and connective tissue mast cell types, especially under pathological conditions.

scholarly journals The presence of mast cell precursors in rat peripheral blood

Blood ◽  
1981 ◽  
Vol 58 (3) ◽  
pp. 544-551
Author(s):  
D Zucker-Franklin ◽  
G Grusky ◽  
N Hirayama ◽  
E Schnipper
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Alcian Blue ◽  
Peripheral Blood ◽  
Periodic Acid ◽  
Phenotypic Expression ◽  
Soft Agar ◽  
Sulfated Polysaccharides ◽  
Periodic Acid Schiff ◽  
Agar Culture

Soft agar culture of mononuclear cell fractions prepared from rat peripheral blood yielded numerous colonies consisting of mast cells. The mast cell nature of the cells was established by ultrastructural and histochemical analyses as well as by the demonstration the the colonies contained histamine and that the cells possessed receptors for the Fc component of IgE. Stringent criteria for the distinction of mast cells from monocytes/macrophages that could have metachromatic inclusions were applied. The alcian-blue-safranin technique delineated the maturation of mast cell granules by showing the loss of alcian-blue and increase in safranin-positive organelles presumed to reflect the increase in N-sulfated polysaccharides representing heparin. The mast cells exhibited low or absent reactions for peroxidase, alpha-naphthyl butyrate, periodic acid Schiff, and Sudan black reacting lipid, whereas macrophages stained in parallel were positive for these substances. Since it is known that extracellular conditions may cause variations in phenotypic expression, the observations have led to the hypothesis that mast cells and macrophages may have a common precursor.

scholarly journals Rapid and specific conversion of precursor interleukin 1 beta (IL-1 beta) to an active IL-1 species by human mast cell chymase.

1991 ◽  
Vol 174 (4) ◽  
pp. 821-825 ◽  
Author(s):  
H Mizutani ◽  
N Schechter ◽  
G Lazarus ◽  
R A Black ◽  
T S Kupper
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Secretory Granules ◽  
Interleukin 1 ◽  
Critical Role ◽  
Biologically Active ◽  
Surrounding Tissue ◽  
Human Mast Cell ◽  
Interleukin 1 Beta ◽  
Mast Cell Chymase

Secretory granules of human dermal mast cells contain a chymotrypsin-like serine proteinase called chymase. In this study, we demonstrate that the inactive cytokine, 31 kD interleukin 1 beta (IL-1 beta), can be converted rapidly to an 18 kD biologically active species by human mast cell chymase. The product formed is three amino acids longer at the amino terminus than the mature IL-1 beta produced by peripheral blood mononuclear cells and has comparable biological activity. Because chymase is a secretory granule constituent, it is likely to be released into the surrounding tissue when mast cells degranulate. It is also known that non-bone marrow derived cells resident in skin (keratinocytes, fibroblasts) produce but do not process 31 kD IL-1 beta. In this context, chymase may be a potent activator of locally produced 31 kD IL-1 beta. Mast cells lie in close apposition to blood vessels in dermis; therefore, chymase mediated conversion of 31 kD IL-1 beta might be expected to have a critical role in the initiation of the inflammatory response in skin.

scholarly journals Distribution of chymase-containing mast cells in human bronchi.

1992 ◽  
Vol 40 (6) ◽  
pp. 781-786 ◽  
Author(s):  
R Matin ◽  
E K Tam ◽  
J A Nadel ◽  
G H Caughey
Keyword(s):  
Mast Cell ◽  
Smooth Muscle ◽  
Mast Cells ◽  
Airway Disease ◽  
Differential Distribution ◽  
Cell Subpopulations ◽  
Mast Cell Chymase ◽  
Tissue Compartments ◽  
Human Bronchi

Mast cell chymase stimulates secretion from cultured airway gland serous cells and hydrolyzes bronchoactive peptides in vitro. To explore the likelihood of these interactions occurring in situ, we examined the distribution and concentration of chymase-containing mast cells near glands and smooth muscle of major human bronchi from eight individuals without known airway disease. Total airway mast cells and the subset of mast cells containing chymase were detected by staining for methylene blue metachromasia and chloroacetate esterase activity, respectively. The percentage of chymase-containing mast cells was found to differ strikingly among bronchial tissue compartments. Near glands, for example, the concentration of chymase-positive mast cells (640 +/- 120 cells/mm3) was 73 +/- 9% that of total mast cells (910 +/- 130 cells/mm3), whereas in smooth muscle the concentration of chymase-positive mast cells (450 +/- 200 cells/mm3) was only 14 +/- 4% that of total mast cells (2920 +/- 620 cells/mm3). Of all chymase-containing mast cells in the airway subepithelium, 30 +/- 4% were located within 20 microns of submucosal glands. Although the percentage of chymase-containing cells varied, the absolute concentration of chymase-containing mast cells was similar in all compartments. These results reveal a differential distribution of mast cell subpopulations in human airway and suggest that mast cells containing chymase are near gland and smooth muscle targets.

scholarly journals TISSUE MAST CELLS AND ACUTE INFLAMMATION IN EXPERIMENTAL CUTANEOUS MUCORMYCOSIS OF NORMAL, 48/80-TREATED, AND DIABETIC RATS

1960 ◽  
Vol 112 (6) ◽  
pp. 1069-1084 ◽  
Author(s):  
Walter H. Sheldon ◽  
Heinz Bauer
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Inflammatory Response ◽  
Alloxan Diabetes ◽  
Acute Inflammation ◽  
Normal Function ◽  
Tissue Mast Cell ◽  
Cytoplasmic Granules ◽  
Cutaneous Mucormycosis ◽  
Fungus Growth

The role of the tissue mast cells in relation to the acute inflammatory reaction to experimental cutaneous mucormycosis was studied histologically in normal rats, in animals whose tissue mast cells had been depleted of their cytoplasmic granules prior to infection by the administration of compound 48/80 and in others in whom acute alloxan diabetes with acidosis had been produced before injection of the fungus. The discharge of the tissue mast cell granules in normal rats occurred within minutes at the site of infection and appeared to initiate the rapid onset of acute inflammation. The degranulation of the tissue mast cells subsided in a short time and the cells reassumed a normal histologic appearance while inflammation progressed with the formation of circumscribed lesions. In animals pretreated with compound 48/80 in which the tissue mast cells contained no granules, the onset of inflammation was briefly delayed, the intensity of the process was somewhat decreased, fibroblastic proliferation was retarded, and the fungus growth in the early lesions was increased. However, the infection did not spread and the lesions were well localized. The tissue mast cells in the diabetic and acidotic rats completely failed to discharge their cytoplasmic granules, the onset and intensity of the acute inflammatory response were markedly delayed and decreased and the infection progressed rapidly with massive fungus growth invading adjacent tissues. A relationship between the discharged tissue mast cell granules and eosinophilic granulocytes was noted since the latter were numerous among the inflammatory cell exudate in normal rats and scarce in the lesions of the diabetic animals. It is concluded that a function of the tissue mast cells in the normal rat is the rapid initiation of acute inflammation at the site of injury and that degranulation of these cells prior to infection somewhat delays the inflammatory response and therefore slightly diminishes host resistance. Furthermore, a severe metabolic disorder such as acute alloxan diabetes with acidosis, inhibits the normal function of the tissue mast cells, delays and decreases inflammation, and in this manner contributes to the greatly increased susceptibility of the host to infection.

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