scholarly journals Estrogen is an important mediator of mast cell activation in ovarian endometriomas

Reproduction ◽  
2018 ◽  
Vol 155 (1) ◽  
pp. 73-83 ◽  
Author(s):  
Tian-Hong Zhu ◽  
Shao-Jie Ding ◽  
Tian-Tian Li ◽  
Li-Bo Zhu ◽  
Xiu-Feng Huang ◽  
...  

Endometriosis is an estrogen-dependent disease. Previous research has shown that abnormal enzymes associated with estrogen (E2) metabolism and an increased number of mast cells (MCs) in endometriomas are implicated in the pathogenesis of endometriosis. However, it remains unclear how MCs mediate the role of E2 in endometriosis. Accordingly, we investigated whether E2 was associated with the number of MCs, and the rate of degranulation, in local ovarian endometriomas, as well as the role of E2 on MCs during the pathogenesis of endometriosis. Using enzyme-linked immunosorbent assay and immunohistochemistry, we found that concentrations of E2, and the number and activity of MCs, were significantly higher in ovarian endometriomas than in controls, and that these parameters were correlated with the severity of endometriosis-associated dysmenorrhea. By measuring the release of hexosaminidase, we found that the rate of RBL2H3 cell degranulation increased after E2 treatment. Furthermore, activation of RBL2H3 cells by E2 was found to trigger the release of biologically active nerve growth factor, which promotes neurite outgrowth in PC12 cells and also sensitizes dorsal root ganglion cells via upregulation ofNav1.8and transient receptor potential cation channel (subfamily V member 1) expression levels. When treated with E2, endometriotic cells could promote RBL2H3 cell recruitment by upregulating expression levels of stem cell factor, transforming growth factor-β and monocyte chemoattractant protein-1; these observations were not evident with control endometrial cells. Thus, elevated E2 concentrations may be a key factor for degranulation and recruitment of MCs in ovarian endometriomas, which play a key role in endometriosis-associated dysmenorrhea.

2000 ◽  
Vol 85 (12) ◽  
pp. 4781-4788 ◽  
Author(s):  
A. G. Moore ◽  
D. A. Brown ◽  
W. D. Fairlie ◽  
A. R. Bauskin ◽  
P. K. Brown ◽  
...  

Macrophage inhibitory cytokine-1 (MIC-1) is a recently described divergent member of the transforming growth factor-β superfamily. MIC-1 transcription up-regulation is associated with macrophage activation, and this observation led to its cloning. Northern blots indicate that MIC-1 is also present in human placenta. A sensitive sandwich enzyme-linked immunosorbent assay for the quantification of MIC-1 was developed and used to examine the role of this cytokine in pregnancy. High levels of MIC-1 are present in the sera of pregnant women. The level rises substantially with progress of gestation. MIC-1 can also be detected, in large amounts, in amniotic fluid and placental extracts. In addition, the BeWo placental trophoblastic cell line was found to constitutively express the MIC-1 transcript and secrete large amounts of MIC-1. These findings suggest that the placental trophoblast is a major source of the MIC-1 present in maternal serum and amniotic fluid. We suggest that MIC-1 may promote fetal survival by suppressing the production of maternally derived proinflammatory cytokines within the uterus.


2017 ◽  
Vol 5 (2) ◽  
Author(s):  
Rita Shintawati ◽  
Sunarjati Sudigdoadi ◽  
Tita Husnitawati Madjid ◽  
Endang Sutedja

This research aims to see the effect of L.plantarum in modulating the secretion of Transforming Growth Factor-TGFβ1, TGFβ3 macrophages and fibroblasts, Interferon-IFNα macrophages, and to analyze the possibility of L.plantarum potency in supporting the process of scarless wound healing. The culture of peritoneal macrophages was treated with L.plantarum for 24 hours, while another macrophage was S.aureus stimulated for 6 hours before treatment of L.plantarum for 24 hours. The formed supernatant was separated and centrifuged to serve as a treatment on the culture of rat dermal fibroblasts for 24 hours. The supernatant was then separated and centrifuged; its cytokine level was measured with enzyme-linked immunosorbent assay-ELISA. Treatment of L.plantarum with medium and high doses increased the secretion of IFNa macrophages compared with the control; all L.plantarum doses can stimulate the secretion of TGFβ1 fibroblast and TGFβ3 macrophage significantly, but it does not affect the secretion of TGFβ1 macrophages. It can be concluded that L.plantarum increased the secretion of IFNα macrophages higher than the treatment preceded by S.aureus stimulation. The secretion of TGFβ1 fibroblasts and TGFβ3 fibroblasts also increased, but it was not as high as L.plantarum treatment stimulated by S.aureus. Therefore, the application of L.plantarum to support the process of wound healing, prophylactic of the excessive scar and fibrosis can be researched further.


2010 ◽  
Vol 10 (3) ◽  
pp. 204-209 ◽  
Author(s):  
Xiao-Zhi Zheng ◽  
Lian-Fang Du ◽  
Hui-Ping Wang

Proliferative vitreoretinopathy (PVR) is a serious complication of retinal detachment surgery or ocular trauma. Our previous study indicated that intravitreal co-injection of retinal pigmented epithelial (RPE) -J cells and platelet-rich plasma (PRP) (not RPE-J cells or PRP alone) in Wistar rat eyes can successfully induce a model of PVR. But which cells are involved in this process and why different induction methods, intravitreal injection of RPE-J cells or/and PRP, induced a different situation remain to be unknown. In this study, immunohistochemistry was performed to identify the main cell types involved in this process. The expression levels of transforming growth factor (TGF) -β2, platelet-derived growth factor (PDGF)- AA and PDGF-BB were tested using enzyme-linked immunosorbent assay (ELISA)The results showed that RPE cells, glial cells, fibroblasts and macrophages took part in the pathogenesis of this model. The expression levels and durations of TGF^2 and PDGF-BB partially explained the different results induced by the different induction methods. This provides an experimental proof for attenuation of the experimental PVR by targeting at a specific cells or growth factor.


2007 ◽  
Vol 21 (4) ◽  
pp. 389-394 ◽  
Author(s):  
Huabin Li ◽  
Hongyan Jiang ◽  
Lei Cheng ◽  
Yun Oh ◽  
Geng Xu

Background Chronic rhinosinusitis (CRS) may cover different disease entities, and the pathogenic mechanism remains unclear. Methods The aim of this study was to evaluate the expression of chloride channel protein CLC-2 and CLC-3 in CRS without nasal polyps (CRSsNP) and evaluate the roles of interleukin (IL)-4 and transforming growth factor (TGF) beta in the up-regulation of CLC-2 and CLC-3. We detected expression of CLC-2 and CLC-3 in 17 patients with CRSsNP by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR), and we examined the concentration of TGF-beta, IL-4, IL-5, and interferon (IFN) γ in ethmoid sinus mucosa by enzyme-linked immunosorbent assay (ELISA). Results We found that CLC-2 and CLC-3 is up-regulated in CRSnNP and located in submucosal glands and epithelium of the ethmoid sinus. CLC-2 and CLC-3 mRNA correlated with IL-4 in CRSsNP (r = 0.57 and 0.65; p < 0.05). CLC-2 and CLC-3 mRNA correlated negatively with mucosal TGF-beta in CRSsNP (r = -0.49 and -0.54; p < 0.05). Conclusion We concluded that CLC-2 and CLC-3 is up-regulated in ethmoid mucosa and may affect the development of CRSsNP. TGF-beta and IL-4 may modulate the expression of CLC-2 and CLC-3 in CRSsNP.


2021 ◽  
Vol 2021 (2) ◽  
pp. 34-42
Author(s):  
V. V. Kachkovska ◽  
A. V. Kovchun ◽  
A. M. Bondarkova ◽  
L. N. Prystupa

The goal of our research was to analyze the role of transforming growth factor-β1 (TGF-β1 ) in airway remodeling, inflammation, clinical course, treatment efficacy in patients with bronchial asthma (BA) according to the literature data, as well as determination of this biomarkers level in the blood of BA patients. Material and research methods. The publications is containing the results of studies on the role of TGF-β1 in the course of BA have been analyzed. The level of TGF-β1 in the blood was determined within enzyme-linked immunosorbent assay using kits “IBL International GMBH, Germany” in 553 BA patients and in 95 healthy individuals. Results. The article presents data about TGF-β1 influence on the processes of airway remodeling in BA patients, its role in microcirculation disorders, mucus production, eosinophilic inflammation and severity of clinical symptoms of the disease. The level of TGF-β1 expression was associated with disease control, severity and duration of the disease, despite conflicting data that require further study. In addition, there were presented recent research data about TGF-β1 as a marker of airway remodeling and as a therapeutic target in the treatment of BA patients. Glucocorticoids, tiotropium bromide, methylxanthines, selective inhibitors of TGF-β1 , resveratrol, simvastatin and montelukast and their mechanisms of influence were presented in detail. Significantly higher level of TGF-β1 in the blood of patients with BA was found (38.5 ± 0.7) pg/ml compared with healthy individuals (33.9 ± 1.0) pg /ml, p = 0.007. Conclusion. A significantly higher level of TGF-β1 was revealed in the blood of BA patients. In our opinion, a differentiated analysis of the content of this marker depending on the phenotype of the disease is important, which would explain the conflicting results of different studies, deepen understanding of its pathophysiological and clinical role in order to develop methods for slowing airway remodeling. Key words: bronchial asthma, transforming growth factor-β1 (TGF-β1), airway remodeling.


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