scholarly journals Role of mast cells and protease-activated receptor-2 in cyclooxygenase-2 expression in urothelial cells

2009 ◽  
Vol 297 (4) ◽  
pp. R1127-R1135 ◽  
Author(s):  
Zun-Yi Wang ◽  
Peiqing Wang ◽  
Dale E. Bjorling
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Primary Cultures ◽  
Cyclooxygenase 2 ◽  
Protein Abundance ◽  
Urothelial Cells ◽  
Cellular Mechanisms ◽  
Bladder Inflammation ◽  
Cox 2 ◽  
Protease Activated Receptor 2

Mast cells have been shown to play a role in development and persistence of various inflammatory bladder disorders. Mast cell-derived tryptase specifically activates protease-activated receptor-2 (PAR-2), and PAR-2 is known to be involved in inflammation. We investigated whether mast cells participate in increase of cyclooxygenase-2 (COX-2) protein abundance in urothelium/suburothelium of bladders of mice subsequent to cyclophosphamide (CYP)-induced bladder inflammation. We also used primary cultures of human urothelial cells to investigate cellular mechanisms underlying activation of PAR-2 resulting in increased COX-2 expression. We found that treatment of mice with CYP (150 mg/kg ip) increased COX-2 protein abundance in bladder urothelium/suburothelium 3, 6, and 24 h after CYP ( P < 0.01), and increased COX-2 protein abundance was prevented by treatment of mice with the mast cell stabilizer sodium cromolyn (10 mg/kg ip) for 4 consecutive days before CYP treatment. Incubation of freshly isolated mouse urothelium/suburothelium with a selective PAR-2 agonist, 2-furoyl-LIGRLO-amide (3 μM), also increased COX-2 protein abundance ( P < 0.05). We further demonstrated that 2-furoyl-LIGRLO-amide (3 μM) increased COX-2 mRNA expression and protein abundance in primary cultures of human urothelial cells ( P < 0.01), and the effects of PAR-2 activation were mediated primarily by the ERK1/2 MAP kinase pathway. These data indicate that there are functional interactions among mast cells, PAR-2 activation, and increased expression of COX-2 in bladder inflammation.

scholarly journals Pyroptosis engagement and bladder urothelial cell-derived exosomes recruit mast cells and induce barrier dysfunction of bladder urothelium after uropathogenic E. coli infection

2019 ◽  
Vol 317 (3) ◽  
pp. C544-C555 ◽  
Author(s):  
Zonglong Wu ◽  
Yan Li ◽  
Qinggang Liu ◽  
Yaxiao Liu ◽  
Lipeng Chen ◽  
...  
Keyword(s):  
Mast Cells ◽  
Barrier Function ◽  
Urothelial Cells ◽  
Barrier Dysfunction ◽  
Epithelial Barrier Function ◽  
E Coli ◽  
Bladder Urothelium ◽  
Protease Activated Receptor 2

The specific regulatory mechanism of bladder urothelial barrier dysfunction after infection with uropathogenic Escherichia coli (UPEC) is still unclear. The cross talk between bladder urothelial cells and mast cells may play an important role during UPEC infection. In this study, the pyroptosis of urothelial cells was investigated after UPEC infection both in vivo and in vitro. The levels of IL-1β and IL-18 in exosomes derived from bladder urothelial cells after UPEC infection were detected. The role of these processes in the recruitment and activation of mast cells was measured. The mechanism of mast cell-induced disruption of bladder epithelial barrier function was also assessed. We found that UPEC infection induced pyroptosis of bladder urothelial cells and led to the release of IL-1β and IL-18 in the form of exosomes, which promoted the migration of mast cells. Tryptase secreted by mast cells aggravated the damage to the barrier function of the bladder urothelium by acting on protease-activated receptor 2 (PAR2). Inhibition of pyroptosis or the tryptase-PAR2 axis reduced the disruption of bladder urothelial barrier function and decreased the bacterial burden. The present study supports a novel mechanism by which pyroptosis-dependent release of exosomes from bladder urothelial cells activates mast cells and regulates bladder urothelial barrier function during UPEC infection.

scholarly journals Mast cells and mast cell tryptase enhance migration of human lung fibroblasts through protease-activated receptor 2

2018 ◽  
Vol 16 (1) ◽  
Author(s):  
Mariam Bagher ◽  
Anna-Karin Larsson-Callerfelt ◽  
Oskar Rosmark ◽  
Oskar Hallgren ◽  
Leif Bjermer ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Human Lung ◽  
Lung Fibroblasts ◽  
Mast Cell Tryptase ◽  
Human Lung Fibroblasts ◽  
Protease Activated Receptor 2

A role for mast cells and mast cell tryptase in driving neutrophil recruitment in LPS-induced lung inflammation via protease-activated receptor 2 in mice

2020 ◽  
Vol 69 (10) ◽  
pp. 1059-1070 ◽  
Author(s):  
Aline Dias de Almeida ◽  
Irismara Sousa Silva ◽  
Weslley Fernandes-Braga ◽  
Antônio Carlos Melo LimaFilho ◽  
R odrigo Machado Florentino ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Lung Inflammation ◽  
Neutrophil Recruitment ◽  
Mast Cell Tryptase ◽  
Protease Activated Receptor 2

scholarly journals Intercellular interactions between mast cells and stromal fibroblasts obtained from canine cutaneous mast cell tumours

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lidia H. Pulz ◽  
Yonara G. Cordeiro ◽  
Greice C. Huete ◽  
Karine G. Cadrobbi ◽  
Arina L. Rochetti ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Cell Viability ◽  
Cultured Cells ◽  
Primary Cultures ◽  
Physical Contact ◽  
Cell Contact ◽  
Low Grade ◽  
Stromal Fibroblasts

AbstractMast cell tumours (MCTs) are the most frequent malignant skin neoplasm in dogs. Due to the difficulty in purifying large numbers of canine neoplastic mast cells, relatively little is known about their properties. A reproducible in vitro model is needed to increase the understanding about the phenotype and functional properties of neoplastic mast cells. In the present study, we describe the establishment of primary cocultures of neoplastic mast cells from canine cutaneous MCTs and cancer-associated fibroblasts. We confirmed the inability of canine neoplastic mast cells to remain viable for long periods in vitro without the addition of growth factors or in vivo passages in mice. Using a transwell system, we observed that mast cell viability was significantly higher when there is cell-to-cell contact in comparison to non-physical contact conditions and that mast cell viability was significantly higher in high-grade than in low-grade derived primary cultures. Moreover, the use of conditioned medium from co-cultured cells led to a significantly higher tumoral mast cell viability when in monoculture. Signalling mechanisms involved in these interactions might be attractive therapeutic targets to block canine MCT progression and deserve more in-depth investigations.

Mast cells mediate substance P-induced bladder inflammation through an NK1 receptor-independent mechanism

2002 ◽  
Vol 283 (4) ◽  
pp. F616-F629 ◽  
Author(s):  
Ricardo Saban ◽  
Norma P. Gerard ◽  
Marcia R. Saban ◽  
Ngoc-Bich Nguyen ◽  
Douglas J. DeBoer ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Substance P ◽  
Bone Marrow Cells ◽  
Gene Array ◽  
Bladder Inflammation ◽  
Gene Array Analysis ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Neurokinin 1

The role of neurokinin-1 receptors (NK1R) in the interaction between mast cells and substance P (SP) in bladder inflammation was determined. Mast cell-deficient KitW/KitW-v , congenic normal (+/+), and KitW/KitW-v mice that were reconstituted with bone marrow cells isolated from NK1R−/− mice were challenged by instillation of SP, antigen, or saline into the urinary bladder. Twenty-four hours after challenge, the bladders were prepared for morphological assessment and gene expression. SP-induced bladder inflammation was mast cell dependent and did not require NK1R expression on the mast cell. Cluster analysis identified functionally significant genes that were dependent on the presence of mast cells for their upregulation regardless of stimulus. Those include serine protein inhibitor 2.2, maspin, mitogen- and stress-activated protein kinase 2, and macrophage colony-stimulating factor 1. Our findings demonstrate that while mast cells are essential for both antigen- and SP-induced bladder inflammation, there are common genes and unique genes expressed in each type of inflammatory reaction. When combined with unique animal models, gene array analysis provides a useful approach for identifying and characterizing pathways involved in bladder inflammation.

scholarly journals Correction to: A role for mast cells and mast cell tryptase in driving neutrophil recruitment in LPS-induced lung inflammation via protease-activated receptor 2 in mice

2020 ◽  
Vol 69 (10) ◽  
pp. 1071-1071
Author(s):  
Aline Dias de Almeida ◽  
Irismara Sousa Silva ◽  
Weslley Fernandes-Braga ◽  
Antônio Carlos Melo LimaFilho ◽  
Rodrigo Machado Florentino ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Lung Inflammation ◽  
Neutrophil Recruitment ◽  
Mast Cell Tryptase ◽  
Protease Activated Receptor 2

Assessment of Cyclooxygenase-2 Expression in Canine Hemangiosarcoma, Histiocytic Sarcoma, and Mast Cell Tumor

2005 ◽  
Vol 42 (3) ◽  
pp. 350-353 ◽  
Author(s):  
D. A. Heller ◽  
C. A. Clifford ◽  
M. H. Goldschmidt ◽  
D. E. Holt ◽  
M. J. Manfredi ◽  
...  
Keyword(s):  
Mast Cell ◽  
Histiocytic Sarcoma ◽  
Cyclooxygenase 2 ◽  
Cell Tumor ◽  
University Of Pennsylvania ◽  
Tumor Type ◽  
Mast Cell Tumor ◽  
Grade Ii ◽  
Cox 2 ◽  
The University

To determine whether cyclooxygenase-2 (COX-2) is expressed in canine hemangiosarcoma (HsA), histiocytic sarcoma (Hs), and grade-II mast cell tumor (MCT), we performed immunohistochemistry using COX-2 antibodies in the aforementioned tumors. Twenty cases of each tumor type were selected initially from the Laboratory of Pathology archives of cases submitted through the Matthew J. Ryan Veterinary Hospital of the University of Pennsylvania. Immunohistochemistry was performed, using a polyclonal antiprostaglandin endoperoxide synthase immunoglobulin G COX-2 antibody. Sections from the kidneys of young dogs, in which the macula densa stains positive for COX-2, served as positive controls. Slides were reviewed by a single pathologist (M. H. Goldschmidt) and graded for COX-2 expression according to previously established scales.18 Descriptive data is given for each tumor type. COX-2 expression was identified in 0 of 19 HSA, 1 of 20 HS, and 1 of 17 grade-II MCT. Although COX-2 has been shown to be overexpressed in selected human sarcomas and hematopoeitic tumors, these results indicate that canine HSA, HS, and MCT do not express COX-2 in any appreciable fashion.

scholarly journals Interleukin 3-dependent and -independent mast cells stimulated with IgE and antigen express multiple cytokines.

1989 ◽  
Vol 170 (1) ◽  
pp. 245-257 ◽  
Author(s):  
P R Burd ◽  
H W Rogers ◽  
J R Gordon ◽  
C A Martin ◽  
S Jayaraman ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Wide Spectrum ◽  
Primary Cultures ◽  
Ifn Gamma ◽  
Gm Csf ◽  
Cell Clones ◽  
Relationship Of ◽  
The Relationship

In response to IgE and specific multivalent antigen, mast cell lines (both growth factor-dependent and -independent) induce the transcription and/or secretion of a number of cytokines having a wide spectrum of activities. We have identified IL-1, IL-3, IL-5, IL-6, IFN-gamma, GM-CSF, JE, MIP1 alpha, MIP1 beta, and TCA3 RNA in at least two of four mast cell clones. The production of these products (except JE) is activation-associated and can be induced by IgE plus antigen. In selected instances cytokine expression can also be induced by activation with Con A or phorbol ester plus ionophore, albeit to levels less than those observed with IgE plus antigen. In addition, long-term mast cell clones and primary cultures of bone marrow-derived mast cells specifically release IL-1, IL-4, and/or IL-6 bioactivity after activation. These findings suggest that in addition to their inflammatory effector function mast cells may serve as a source of growth and regulatory factors. The relationship of mast cells to cells of the T lymphocyte lineage is discussed.

Nitric oxide regulates renal cortical cyclooxygenase-2 expression

2000 ◽  
Vol 279 (1) ◽  
pp. F122-F129 ◽  
Author(s):  
Hui-Fang Cheng ◽  
Jun-Ling Wang ◽  
Ming-Zhi Zhang ◽  
James. A. McKanna ◽  
Raymond C. Harris
Keyword(s):  
Nitric Oxide ◽  
Primary Cultures ◽  
Cyclooxygenase 2 ◽  
Macula Densa ◽  
Thick Ascending Limb ◽  
Salt Diet ◽  
Nos Inhibitors ◽  
Low Salt ◽  
Cox 2 ◽  
Arteriolar Tone

We have previously shown that cyclooxygenase-2 (COX-2) is localized to the cortical thick ascending limb of the loop of Henle (cTALH)/macula densa of the rat kidney, and expression increases in response to low-salt diet and/or angiotensin-converting enzyme (ACE) inhibition. Because of the localization of neuronal nitric oxide synthase (nNOS) to macula densa and surrounding cTALH, the present study investigated the role of nitric oxide (NO) in the regulation of COX-2 expression. For in vivo studies, rats were fed a normal diet, low-salt diet or low-salt diet combined with the ACE inhibitor captopril. In each group, one-half of them were treated with the nNOS inhibitors 7-nitroinidazole (7-NI) or S-methyl-thiocitrulline. Both of these NOS inhibitors inhibited increases in COX-2 mRNA and immunoreactive protein in response to low salt and low salt+captopril. For in vitro studies, COX-2 expression was studied in primary cultures of rabbit cTALH cells immunodisssected with Tamm-Horsfall antibody. Basal COX-2 immunoreactivity expression was stimulated by S-nitroso- N-acetyl-penicillamine (SNAP), an NO donor, and intracellular cGMP concentration. The cultured cells expressed immunoreactive nNOS, and 7-NI inhibited basal COX-2 immunoreactivity expression, which could be partially overcome by cGMP. In summary, these studies indicate that NO is a mediator of increased renal cortical COX-2 expression seen in volume depletion and suggest important interactions between the NO and COX-2 systems in the regulation of arteriolar tone and the renin-angiotensin system by the macula densa.

Sign in / Sign up

Export Citation Format

Share Document