scholarly journals Catechin synergistically potentiates mast cell-stabilizing property of caffeine

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Misaki Yashima ◽  
Yukine Sato ◽  
Itsuro Kazama
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Suppressive Effect ◽  
Low Concentrations ◽  
Peritoneal Mast Cells ◽  
Anti Cancer ◽  
Health Promoting ◽  
Anti Oxidant ◽  
First Time ◽  
Allergic Disorders

AbstractCaffeine and catechin, contained in coffee and tea, are commonly consumed substances worldwide. Studies revealed their health promoting functions, such as anti-oxidant, anti-cancer and anti-bacterial properties. Additionally, studies also revealed their roles in ameliorating the symptoms of allergic disorders, indicating their anti-allergic properties. In the present study, using the differential-interference contrast (DIC) microscopy, we examined the effects of caffeine and catechin on the degranulation from rat peritoneal mast cells. Both caffeine and catechin dose-dependently decreased the numbers of degranulating mast cells. At concentrations equal to or higher than 25 mM, caffeine and catechin markedly suppressed the numbers of degranulating mast cells. In contrast, at relatively lower concentrations, both substances did not significantly affect the numbers of degranulating mast cells. However, surprisingly enough, low concentrations of catechin (1, 2.5 mM) synergistically enhanced the suppressive effect of 10 mM caffeine on mast cell degranulation. These results provided direct evidence for the first time that caffeine and catechin dose-dependently inhibited the process of exocytosis. At relatively lower concentrations, caffeine or catechin alone did not stabilize mast cells. However, low concentrations of catechin synergistically potentiated the mast cell-stabilizing property of caffeine.

Clarithromycin Dose-Dependently Stabilizes Rat Peritoneal Mast Cells

Chemotherapy ◽  
2016 ◽  
Vol 61 (6) ◽  
pp. 295-303 ◽  
Author(s):  
Itsuro Kazama ◽  
Kazutomo Saito ◽  
Asuka Baba ◽  
Tomohiro Mori ◽  
Nozomu Abe ◽  
...  
Keyword(s):  
Mast Cell ◽  
Plasma Membrane ◽  
Mast Cells ◽  
Water Soluble ◽  
Patch Clamp Technique ◽  
Membrane Deformation ◽  
Whole Cell Patch Clamp ◽  
Peritoneal Mast Cells ◽  
Rat Peritoneal Mast Cells ◽  
First Time

Background: Macrolides, such as clarithromycin, have antiallergic properties. Since exocytosis in mast cells is detected electrophysiologically via changes in membrane capacitance (Cm), the absence of such changes due to the drug indicates its mast cell-stabilizing effect. Methods: Employing the whole-cell patch clamp technique in rat peritoneal mast cells, we examined the effects of clarithromycin on Cm during exocytosis. Using a water-soluble fluorescent dye, we also examined its effect on deformation of the plasma membrane. Results: Clarithromycin (10 and 100 μM) significantly inhibited degranulation from mast cells and almost totally suppressed the GTP-γ-S-induced increase in Cm. It washed out the trapping of the dye on the surface of mast cells. Conclusions: This study provides for the first time electrophysiological evidence that clarithromycin dose-dependently inhibits the process of exocytosis. The mast cell-stabilizing action of clarithromycin may be attributable to its counteractive effect on plasma membrane deformation induced by exocytosis.

Antiapoptotic function of Bcl-2 in mast cells is dependent on its association with heat shock protein 90β

Blood ◽  
2006 ◽  
Vol 107 (4) ◽  
pp. 1413-1420 ◽  
Author(s):  
Cellina Cohen-Saidon ◽  
Irit Carmi ◽  
Avishai Keren ◽  
Ehud Razin
Keyword(s):  
Mast Cell ◽  
Rna Interference ◽  
Mast Cells ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Caspase 3 ◽  
Caspase 7 ◽  
Antiapoptotic Activity ◽  
Novel Strategy ◽  
First Time

In the present study, we demonstrated that the antiapoptotic function of Bcl-2 in mast cells is significantly dependent on its association with the heat shock protein 90β (Hsp90β). Dissociation of these 2 proteins inhibits the antiapoptotic activity of Bcl-2 by initiating the release of cytochrome c from mitochondria into cytosol and increasing the activity of caspase 3 and caspase 7, resulting in mast-cell apoptosis. The antiapoptotic activity of Bcl-2 was greatly affected by knocking-out specifically Hsp90β using the RNA interference approach. Thus, for the first time, it has been shown that Hsp90β might modulate the antiapoptotic activity of Bcl-2 at least in mast cells. These findings could have implications for a novel strategy of regulating apoptosis in patients with mastocytosis and other mast cell–associated diseases.

IgE Receptors from Rat Intestinal Mucosal and Peritoneal Mast Cells Show Mast Cell Subtype-Specific Differences

1989 ◽  
Vol 88 (1-2) ◽  
pp. 200-202
Author(s):  
M. Swieter ◽  
B.M.C. Chan ◽  
T.D.G. Lee ◽  
C.J. Rimmer ◽  
A. Froese ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Subtype ◽  
Ige Receptors ◽  
Peritoneal Mast Cells

scholarly journals Multiple bidirectional alterations of phenotype and changes in proliferative potential during the in vitro and in vivo passage of clonal mast cell populations derived from mouse peritoneal mast cells

Blood ◽  
1988 ◽  
Vol 72 (3) ◽  
pp. 877-885 ◽  
Author(s):  
Y Kanakura ◽  
H Thompson ◽  
T Nakano ◽  
T Yamamura ◽  
H Asai ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Tissue Type ◽  
Cell Populations ◽  
Proliferative Potential ◽  
Heparin Binding ◽  
Peritoneal Mast Cells ◽  
Proliferative Ability

Mouse peritoneal mast cells (PMC) express a connective tissue-type mast cell (CTMC) phenotype, including reactivity with the heparin-binding fluorescent dye berberine sulfate and incorporation of [35S] sulfate predominantly into heparin proteoglycans. When PMC purified to greater than 99% purity were cultured in methylcellulose with IL-3 and IL-4, approximately 25% of the PMC formed colonies, all of which contained both berberine sulfate-positive and berberine sulfate-negative mast cells. When these mast cells were transferred to suspension culture, they generated populations that were 100% berberine sulfate-negative, a characteristic similar to that of mucosal mast cells (MMC), and that synthesized predominantly chondroitin sulfate [35S] proteoglycans. When “MMC-like” cultured mast cells derived from WBB6F1-+/+ PMC were injected into the peritoneal cavities of mast cell-deficient WBB6F1- W/Wv mice, the adoptively transferred mast cell population became 100% berberine sulfate-positive. In methylcellulose culture, these “second generation PMC” formed clonal colonies containing both berberine sulfate-positive and berberine sulfate-negative cells, but exhibited significantly less proliferative ability than did normal +/+ PMC. Thus, clonal mast cell populations initially derived from single PMC exhibited multiple and bidirectional alterations between CTMC-like and MMC-like phenotypes. However, this process was associated with a progressive diminution of the mast cells' proliferative ability.

scholarly journals Changes in numbers and types of mast cell colony-forming cells in the peritoneal cavity of mice after injection of distilled water: evidence that mast cells suppress differentiation of bone marrow-derived precursors

Blood ◽  
1988 ◽  
Vol 71 (3) ◽  
pp. 573-580 ◽  
Author(s):  
Y Kanakura ◽  
A Kuriu ◽  
N Waki ◽  
T Nakano ◽  
H Asai ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mast Cell ◽  
Mast Cells ◽  
Peritoneal Cavity ◽  
Bone Marrow Cells ◽  
Water Injection ◽  
Lymphoid Cells ◽  
Distilled Water ◽  
Peritoneal Mast Cells ◽  
Chediak Higashi Syndrome

Abstract Two different types of cells in the peritoneal cavity of mice produce mast cell colonies in methylcellulose. “Large” mast cell colonies are produced by bone marrow-derived precursors resembling lymphoid cells by light microscopy (L-CFU-Mast), whereas “medium” and “small” mast cell colonies are produced by morphologically identifiable mast cells (M-CFU- Mast and S-CFU-Mast, respectively). In the present study we eradicated peritoneal mast cells by intraperitoneal (IP) injection of distilled water. The regeneration process was investigated to clarify the relationship between L-CFU-Mast, M-CFU-Mast, and S-CFU-Mast. After injection of distilled water, M-CFU-Mast and S-CFU-Mast disappeared, but L-CFU-Mast increased, and then M-CFU-Mast and S-CFU-Mast appeared, suggesting the presence of a hierarchic relationship. When purified peritoneal mast cells were injected two days after the water injection, the L-CFU-Mast did not increase. In the peritoneal cavity of WBB6F1-+/+ mice that had been lethally irradiated and rescued by bone marrow cells of C57BL/6-bgJ/bgJ (beige, Chediak-Higashi syndrome) mice, L-CFU-Mast were of bgJ/bgJ type, but M-CFU-Mast and S-CFU-Mast were of +/+ type. The injection of distilled water to the radiation chimeras resulted in the development of bgJ/bgJ-type M-CFU-Mast and then S-CFU-Mast. The presence of mast cells appeared to suppress the recruitment of L-CFU- Mast from the bloodstream and to inhibit the differentiation of L-CFU- Mast to M-CFU-Mast.

scholarly journals The Flavonoid Metabolite 2,4,6-Trihydroxybenzoic Acid Is a CDK Inhibitor and an Anti-Proliferative Agent: A Potential Role in Cancer Prevention

Cancers ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 427 ◽  
Author(s):  
Ranjini Sankaranarayanan ◽  
Chaitanya Valiveti ◽  
D. Kumar ◽  
Severine Van slambrouck ◽  
Siddharth Kesharwani ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cancer Cell Proliferation ◽  
Cyclin Dependent Kinase ◽  
Specific Amino Acid ◽  
In Silico Studies ◽  
Anti Cancer ◽  
Anti Oxidant ◽  
First Time ◽  
Related Compounds

Flavonoids have emerged as promising compounds capable of preventing colorectal cancer (CRC) due to their anti-oxidant and anti-inflammatory properties. It is hypothesized that the metabolites of flavonoids are primarily responsible for the observed anti-cancer effects owing to the unstable nature of the parent compounds and their degradation by colonic microflora. In this study, we investigated the ability of one metabolite, 2,4,6-trihydroxybenzoic acid (2,4,6-THBA) to inhibit Cyclin Dependent Kinase (CDK) activity and cancer cell proliferation. Using in vitro kinase assays, we demonstrated that 2,4,6-THBA dose-dependently inhibited CDKs 1, 2 and 4 and in silico studies identified key amino acids involved in these interactions. Interestingly, no significant CDK inhibition was observed with the structurally related compounds 3,4,5-trihydroxybenzoic acid (3,4,5-THBA) and phloroglucinol, suggesting that orientation of the functional groups and specific amino acid interactions may play a role in inhibition. We showed that cellular uptake of 2,4,6-THBA required the expression of functional SLC5A8, a monocarboxylic acid transporter. Consistent with this, in cells expressing functional SLC5A8, 2,4,6-THBA induced CDK inhibitory proteins p21Cip1 and p27Kip1 and inhibited cell proliferation. These findings, for the first time, suggest that the flavonoid metabolite 2,4,6-THBA may mediate its effects through a CDK- and SLC5A8-dependent pathway contributing to the prevention of CRC.

Dural mast cell degranulation is a putative mechanism for headache induced by PACAP-38

Cephalalgia ◽  
2012 ◽  
Vol 32 (4) ◽  
pp. 337-345 ◽  
Author(s):  
Michael Baun ◽  
Martin Holst Friborg Pedersen ◽  
Jes Olesen ◽  
Inger Jansen-Olesen
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Adenylate Cyclase ◽  
Phospholipase C ◽  
Dura Mater ◽  
Mast Cell Degranulation ◽  
Peritoneal Mast Cell ◽  
Selective Blockade ◽  
Peritoneal Mast Cells

Background: Pituitary adenylate cyclase activating peptide-38 (PACAP-38) has been shown to induce migraine in migraineurs, whereas the related peptide vasoactive intestinal peptide (VIP) does not. In the present study we examine the hypothesis that PACAP-38 and its truncated version PACAP-27 but not VIP cause degranulation of mast cells in peritoneum and in dura mater. Methods: The degranulatory effects of PACAP-38, PACAP-27 and VIP were investigated by measuring the amount of N-acetyl-β-hexosaminidase released from isolated peritoneal mast cells and from dura mater attached to the skull of the rat in vitro. In peritoneal mast cells N-truncated fragments of PACAP-38 (PACAP(6–38), PACAP(16–38) and PACAP(28–38)) were also studied. To investigate transduction pathways involved in mast cell degranulation induced by PACAP-38, PACAP-27 and VIP, the phospholipase C inhibitor U-73122 and the adenylate cyclase inhibitor SQ 22536 were used. Results: The peptides induced degranulation of isolated peritoneal mast cells of the rat with the following order of potency: PACAP-38 = PACAP(6–38) = PACAP(16–38) » PACAP-27 = VIP = PACAP(28–38). In the dura mater we found that 10−5 M PACAP-38 was significantly more potent in inducing mast cell degranulation than the same concentration of PACAP-27 or VIP. Inhibition of intracellular mechanisms demonstrated that PACAP-38-induced degranulation is mediated by the phospholipase C pathway. Selective blockade of the PAC1 receptor did not attenuate degranulation. Conclusion: These findings correlate with clinical studies and support the hypothesis that mast cell degranulation is involved in PACAP-induced migraine. PACAP-38 has a much stronger degranulatory effect on rat peritoneal and dural mast cells than VIP and PACAP-27. The difference in potency between PACAP-38- and PACAP-27/VIP-induced peritoneal mast cell degranulation is probably not related to the PAC1 receptor but is caused by a difference in efficacy on phospholipase C.

Sign in / Sign up

Export Citation Format

Share Document