Cerebral vasospasm: presence of mast cells in human cerebral arteries after aneurysm rupture

1981 ◽  
Vol 54 (6) ◽  
pp. 733-735 ◽  
Author(s):  
Luiz C. M. Faleiro ◽  
Conceição R. S. Machado ◽  
Amado Gripp ◽  
Rubens A. Resende ◽  
Pedro A. Rodrigues

✓ Mast cells contain heparin, histamine, hydrolytic enzymes, and possibly serotonin in metachromatic cytoplasmic granules, and are not visualized in routine histological preparations. Special fixation, frozen sections, and toluidine blue staining are essential for counting the number of mast cells in tissue sections. Histological preparations for counting mast cells were made from arteries of the circle of Willis in persons who died after chest or abdominal trauma (control group) and in patients who had subarachnoid hemorrhage (SAH) after aneurysm rupture. The arteries were removed within 6 hours of death, taking care to avoid damage to their structure, and were immersed in the fixative solution. This preliminary note, reporting findings in only a few cases, is justified by the interesting discovery of a marked increase in mast cell population in the muscular layer of arteries after SAH. The series is small because of the difficulty in obtaining suitable material, since mast cells virtually disappear when autopsy is performed later than 6 hours after death. It is concluded from this study that there is an increase of mast cell population in cerebral arterial walls after SAH, mainly in the muscular layer, and that the number of mast cells is higher in arteries closer to the aneurysm.

2021 ◽  
Vol 9 (4) ◽  
pp. 84-89
Author(s):  
V. V. Shishkina ◽  
S. V. Klochkova ◽  
N. T. Alexeeva ◽  
M. Yu. Soboleva ◽  
D. I. Esaulenko ◽  
...  

Mast cells cyclically synthesize and excrete a wide range of biogenesis products with different biological activities into the extracellular matrix and are regulators of local homeostasis both in normal conditions and in pathology – inflammation, oncogenesis, etc. The relative specificity of classical histochemical methods for detecting mast cells in relation to chromogenic to substrates causes certain difficulties in the selective study of the components of the secretome of mast cells, for example, heparin, histamine, chymase or tryptase. Therefore, immunomorphological techniques have become very popular, which identify specific substrates and allow differentiation of the components of the mast cell secretome. Mediators produced by mast cells promote neoangiogenesis, fibrillogenesis and re-epithelialization during the repair process.The aim of our work was to study the tryptase profile of the mast cell population of rat skin during the wound processusing an original combined method of immunohistochemical staining.Material and methods. The experiment involved 12 Wistar rats divided into two groups – intact (n=6) and with the existing wound process of the skin in the withers (n=6). The tryptase profile of mast cells was assessed on the 7th day of the wound process in comparison with the control group.Results. The results obtained showed a significant increase in the number of tryptase-positive mast cells on the 7th day of the wound process in the skin against the background of a general increase in the population of mast cells. Intragranular tryptase reserve was significantly increased. In contrast to the control, where mast cells with single tryptase-positive granules dominated, during the wound process, cells of this type were practically not detected in the skin (43.69±2.9% and 8.55±0.9%). The content of tryptase-positive mast cells with complete filling of the cytoplasm in the control group and the group of animals with a wound process was 14.24±1.2% and 38.03±2.9%, respectively.Conclusion. Thus, when modeling a wound, an increase in tryptase synthesis is detected both in individual MCs and within the entire MC population. This fact indicates that mast cell proteases can become a potential therapeutic target for improving wound regeneration by correcting immunogenesis, inflammation and fiber formation.


Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 334 ◽  
Author(s):  
Kritikou ◽  
Depuydt ◽  
de Vries ◽  
Mulder ◽  
Govaert ◽  
...  

The presence of mast cells in human atherosclerotic plaques has been associated with adverse cardiovascular events. Mast cell activation, through the classical antigen sensitized-IgE binding to their characteristic Fcε-receptor, causes the release of their cytoplasmic granules. These granules are filled with neutral proteases such as tryptase, but also with histamine and pro-inflammatory mediators. Mast cells accumulate in high numbers within human atherosclerotic tissue, particularly in the shoulder region of the plaque. These findings are largely based on immunohistochemistry, which does not allow for the extensive characterization of these mast cells and of the local mast cell activation mechanisms. In this study, we thus aimed to develop a new flow-cytometry based methodology in order to analyze mast cells in human atherosclerosis. We enzymatically digested 22 human plaque samples, collected after femoral and carotid endarterectomy surgery, after which we prepared a single cell suspension for flow cytometry. We were able to identify a specific mast cell population expressing both CD117 and the FcεR, and observed that most of the intraplaque mast cells were activated based on their CD63 protein expression. Furthermore, most of the activated mast cells had IgE fragments bound on their surface, while another fraction showed IgE-independent activation. In conclusion, we are able to distinguish a clear mast cell population in human atherosclerotic plaques, and this study establishes a strong relationship between the presence of IgE and the activation of mast cells in advanced atherosclerosis. Our data pave the way for potential therapeutic intervention through targeting IgE-mediated actions in human atherosclerosis.


1960 ◽  
Vol 38 (1) ◽  
pp. 585-589 ◽  
Author(s):  
Pierre Bois ◽  
Ernest H. Byrne ◽  
Leonard F. Bélanger

The decrease in subcutaneous mast cell population observed in rats on a magnesium-deficient diet has been confirmed. Pretreatment with histamine liberator compound 48/80 accentuates the decrease in mast cell counts. This condition was apparently the result of defective regeneration. The decrease in the number of subcutaneous mast cells was accompanied by a parallel reduction of histamine as appreciated by the guinea pig ileum assay. The peripheral vasodilation, which is an early sign of magnesium deficiency, did not appear in rats pretreated with 48/80.


1960 ◽  
Vol 38 (6) ◽  
pp. 585-589 ◽  
Author(s):  
Pierre Bois ◽  
Ernest H. Byrne ◽  
Leonard F. Bélanger

The decrease in subcutaneous mast cell population observed in rats on a magnesium-deficient diet has been confirmed. Pretreatment with histamine liberator compound 48/80 accentuates the decrease in mast cell counts. This condition was apparently the result of defective regeneration. The decrease in the number of subcutaneous mast cells was accompanied by a parallel reduction of histamine as appreciated by the guinea pig ileum assay. The peripheral vasodilation, which is an early sign of magnesium deficiency, did not appear in rats pretreated with 48/80.


1994 ◽  
Vol 207 (3) ◽  
pp. 274-277 ◽  
Author(s):  
D. A. Schuschke ◽  
J. T. Saari ◽  
C. A. West ◽  
F. N. Miller

2000 ◽  
Vol 113 (18) ◽  
pp. 3289-3298 ◽  
Author(s):  
A. Dragonetti ◽  
M. Baldassarre ◽  
R. Castino ◽  
M. Demoz ◽  
A. Luini ◽  
...  

Basophils and mast cells contain a peculiar class of inflammatory granules that discharge their content upon antigen-mediated crosslinking of IgE-membrane receptors. The pathways for granule biogenesis and exocytosis in these cells are still largely obscure. In this study we employed the rat basophilic leukemia (RBL)/mast cell line to verify the hypothesis that inflammatory granules share common bioactive molecules and functional properties with lysosomes. We demonstrate that inflammatory granules, as identified by the monoclonal 5G10 antibody (which recognises an integral membrane protein) or by Toluidine Blue staining, have an intralumenal acidic pH, possess lysosomal enzymes and are accessible by fluid-phase and membrane endocytosis markers. In addition, we studied the targeting, subcellular localisation and regulated secretion of the lysosomal aspartic protease cathepsin D (CD) as affected by IgE receptor stimulation in order to obtain information on the pathways for granule biogenesis and exocytosis. Stimulation with DNP-BSA of specific IgE-primed RBL cells led to a prompt release of processed forms of CD, along with other mature lysosomal hydrolases. This release could be prevented by addition of EGTA, indicating that it was dependent on extracellular calcium influx. Antigen stimulation also induced exocytosis of immature CD forms accumulated by ammonium chloride, suggesting the existence of an intermediate station in the pathway for granule biogenesis still sensitive to regulated exocytosis. The targeting of molecules to secretory granules may occur via either a mannose-6-phosphate-dependent or mannose-6-phosphate-independent pathway. We conclude that endosomes and lysosomes in basophils/mast cells can act as regulated secretory granules or actually identify with them.


1998 ◽  
Vol 275 (1) ◽  
pp. G63-G67 ◽  
Author(s):  
Carme Juanola ◽  
Magda Giralt ◽  
Marcel Jiménez ◽  
Marisabel Mourelle ◽  
Patri Vergara

Our aim was to determine if mucosal mast cells could be activated by endogenous CCK and, as a consequence, mediate CCK actions in the small intestine. Rats were prepared for electromyography to record electrical activity in the small intestine. In another group of animals, the duodenum was perfused to measure rat mast cell protease II (RMCP II) as indicative of mast cell degranulation. Endogenous CCK release was induced by administration of soybean trypsin inhibitor (SBTI) in conscious rats or by intraduodenal perfusion of ovalbumin hydrolysate (OVH) in anesthetized rats. CCK concentration was measured by bioassay on pancreatic acini. SBTI in control rats disrupted migrating motor complexes (MMC) for >40 min. In rats treated with the mast cell stabilizer ketotifen, SBTI did not induce any change in the MMC pattern. RMCP II concentration in the duodenal perfusate significantly increased after OVH. Perfusate from ketotifen-treated animals did not show any significant increase in RMCP II values during OVH perfusion, although CCK plasma concentration was not different from the control group. Furthermore, infusion of the CCK-B receptor antagonist L-365,260 significantly blocked the increase of RMCP II concentration after OVH. Our results indicate that mucosal mast cells are degranulated by endogenous CCK release through stimulation of CCK-B receptors. Therefore mucosal mast cells participate in CCK intestinal actions.


2003 ◽  
Vol 16 (1) ◽  
pp. 43-47 ◽  
Author(s):  
M.G. Alexandrakis ◽  
D.S. Kyriakou ◽  
D. Seretakis ◽  
W. Boucher ◽  
R. Letourneau ◽  
...  

Mast cells play an important role in allergic inflammation by releasing histamine, tryptase and several inflammatory cytokines. Human leukemic mast cells (HMC-1) have been used to study mast cell mediators and their role in inflammatory mechanisms. HMC-1 contain and release several inflammatory mediators, of which the proteolytic enzyme tryptase is most characteristic. Retinoids, including retinoic acid, are naturally occurring and synthetic derivatives of vitamin A. All-trans-retinoic (ATRA) acid had been previously reported to inhibit cell proliferation, differentiation and apoptosis. In the present study, we investigated the effect of ATRA on the proliferation and secretion of tryptase in HMC-1. HMC-1 were treated with ATRA at 10-4M, 10-5M or 10-6M for 3,4 or 5 days in culture. Control HMC-1 were treated with equal amount of culture medium only. ATRA decreased the number of HMC-1 as compared to the control group. The same treatment for 3, 4 or 5 days also decreased intracellular tryptase levels. These results indicate that ATRA significantly inhibits both proliferation and growth as shown by the decreased intracellular tryptase levels in HMC-1. ATRA may be a useful agent in the treatment of mast cell proliferative disorders.


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