scholarly journals Estrogen Promotes Pituitary Prolactinoma by Upregulating TLR4 / NF-κB/p38MAPK Pathway

2021 ◽  
Author(s):  
Yu Zhang ◽  
Qiaoyan Ding ◽  
Shuman Wang ◽  
Qi Wu ◽  
Ping Ni ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
In Vitro Study ◽  
Tlr4 Expression ◽  
Immunofluorescence Analysis ◽  
Immunohistochemistry Analysis ◽  
P38mapk Pathway ◽  
Interfering Rna ◽  
Harmful Effects

Abstract Background: Prolactinomas have harmful effects on human health, and the pathogenesis is still unknown. Furthermore, the morbidity of women is much more than man, maybe related with estradiol level. Thus, it is important to reveal the pathogenesis and develop new therapeutic methods for prolactinomas.Methods: Immunofluorescence analysis or Immunohistochemistry analysis were performed on the ERβ, TLR4 and prolactin (PRL) expressions of pituitary gland in C57BL/6 mice and human prolactinoma specimen. In the present study, the role of TLR4 in prolactinoma was determined using estradiol-induced mice models in C57BL/6 wild-type (WT) and TLR4−/− mice. MMQ cells were treated with estradiol, fulvestrant, LPS or transfected with different TLR4 small interfering RNA, which to study ERβ, TLR4 and PRL expression in MMQ cells. Co‑immunoprecipitates analysis was used to investigate the interaction between ERβ and TLR4.Results: Immunofluorescence analysis or Immunohistochemistry analysis showed that PRL and TLR4 expression were co-located and increased in the pituitary gland of mice and human prolactinoma specimen compared with the control specimen. It was shown that PRL and TLR4 expression was co-located and increased significantly in the pituitary gland of estradiol-injected prolactinoma mice compared with the control mice. Knockout of TLR4 significantly inhibited tumor overgrowth, and PRL expression was decreased in estradiol-induced mice through regulating TLR4/NF‑κB/p38MAPK pathway. Estradiol promoted PRL expression through regulating TLR4/NF‑κB/p38MAPK pathway in vitro study, and pre-Inhibiting ERβ or TLR4 reverse the effect, while simultaneously activating ERβ and TLR4 enhanced PRL expression than activating single ERβ or TLR4. Furthermore, ERβ co-immunoprecipitates with endogenous TLR4 was assessed by co-immunoprecipitation analysis.Conclusions: These results suggest that estradiol promoted prolactinoma development by activating the TLR4/NF‑κB/ p38MAPK pathway through Erβ and TLR4 knockout inhibited the proliferation and secretion of prolactin in prolactinoma.

scholarly journals Role of glyoxalases in wound healing process: an in vitro study

2021 ◽  
Vol 165 ◽  
pp. 39
Author(s):  
Francesca Lombardi ◽  
Silvano Santini ◽  
Paola Palumbo ◽  
Valeria Cordone ◽  
Virginio Bignotti ◽  
...  
Keyword(s):  
Wound Healing ◽  
Healing Process ◽  
In Vitro Study ◽  
Vitro Study ◽  
Wound Healing Process

scholarly journals Genotoxicity and inflammatory potential of stainless steel welding fume particles: an in vitro study on standard vs Cr(VI)-reduced flux-cored wires and the role of released metals

2021 ◽  
Author(s):  
Sarah McCarrick ◽  
Valentin Romanovski ◽  
Zheng Wei ◽  
Elin M. Westin ◽  
Kjell-Arne Persson ◽  
...  
Keyword(s):  
Dna Damage ◽  
In Vitro Study ◽  
Human Monocyte ◽  
Welding Fumes ◽  
Welding Fume ◽  
Increased Risk ◽  
Underlying Mechanisms ◽  
Cored Wires

AbstractWelders are daily exposed to various levels of welding fumes containing several metals. This exposure can lead to an increased risk for different health effects which serves as a driving force to develop new methods that generate less toxic fumes. The aim of this study was to explore the role of released metals for welding particle-induced toxicity and to test the hypothesis that a reduction of Cr(VI) in welding fumes results in less toxicity by comparing the welding fume particles of optimized Cr(VI)-reduced flux-cored wires (FCWs) to standard FCWs. The welding particles were thoroughly characterized, and toxicity (cell viability, DNA damage and inflammation) was assessed following exposure to welding particles as well as their released metal fraction using cultured human bronchial epithelial cells (HBEC-3kt, 5–100 µg/mL) and human monocyte-derived macrophages (THP-1, 10–50 µg/mL). The results showed that all Cr was released as Cr(VI) for welding particles generated using standard FCWs whereas only minor levels (< 3% of total Cr) were released from the newly developed FCWs. Furthermore, the new FCWs were considerably less cytotoxic and did not cause any DNA damage in the doses tested. For the standard FCWs, the Cr(VI) released in cell media seemed to explain a large part of the cytotoxicity and DNA damage. In contrast, all particles caused rather similar inflammatory effects suggesting different underlying mechanisms. Taken together, this study suggests a potential benefit of substituting standard FCWs with Cr(VI)-reduced wires to achieve less toxic welding fumes and thus reduced risks for welders.

scholarly journals TMIC-34. IN VITRO STUDY OF ROLE OF ASTROCYTIC S1P3 IN REGULATING BLOOD-BRAIN/TUMOR BARRIER PERMEABILITY

2017 ◽  
Vol 19 (suppl_6) ◽  
pp. vi250-vi250
Author(s):  
Anurag N Paranjape ◽  
Brunilde Gril ◽  
Stephan Woditschka ◽  
Jeffrey Hanson ◽  
Xiaolin Wu ◽  
...  
Keyword(s):  
Brain Tumor ◽  
In Vitro Study ◽  
Vitro Study ◽  
Barrier Permeability ◽  
Blood Brain

scholarly journals Intercellular communication in the rat anterior pituitary gland: an in vivo and in vitro study

1975 ◽  
Vol 67 (2) ◽  
pp. 469-476 ◽  
Author(s):  
WH Fletcher ◽  
NC Anderson ◽  
JW Everett
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
In Vitro Study ◽  
Anterior Pituitary Gland ◽  
Stimulus Secretion Coupling ◽  
Unpublished Observation ◽  
Cellular Ca

The concept of "stimulus-secretion coupling" suggested by Douglas and co-workers to explain the events related to monamine discharge by the adrenal medulla (5, 7) may be applied to other endocrine tissues, such as adrenal cortex (36), pancreatic islets (4), and magnocellular hypothalamic neurons (6), which exhibit a similar ion-dependent process of hormone elaboration. In addition, they share another feature, that of joining neighbor cells via membrane junctions (12, 26, and Fletcher, unpublished observation). Given this, and the reports that hormone secretion by the pars distalis also involves a secretagogue-induced decrease in membrane bioelectric potential accompanied by a rise in cellular [Ca++] (27, 34, 41), it was appropriate to test the possibility that cells of the anterior pituitary gland are united by junctions.

An in vitro study of the role of docosahexaenoic acid in human tau protein aggregation

2016 ◽  
Vol 35 (14) ◽  
pp. 3176-3181
Author(s):  
Elham Sadat Mostafavi ◽  
Mohammad Ali Nasiri Khalili ◽  
Sirus Khodadadi ◽  
Gholam Hossein Riazi
Keyword(s):  
Docosahexaenoic Acid ◽  
Protein Aggregation ◽  
Tau Protein ◽  
In Vitro Study ◽  
Vitro Study

scholarly journals The Role of Dietary Phytoestrogens and the Nuclear Receptor PPARγ in Adipogenesis: An in Vitro Study

2019 ◽  
Vol 127 (3) ◽  
pp. 037007 ◽  
Author(s):  
Julie M. Hall ◽  
Heather R. Powell ◽  
Lara Rajic ◽  
Kenneth S. Korach
Keyword(s):  
Nuclear Receptor ◽  
In Vitro Study ◽  
Vitro Study

scholarly journals HIF-1α Activation Promotes Luteolysis by Enhancing ROS Levels in the Corpus Luteum of Pseudopregnant Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Zonghao Tang ◽  
Jiajie Chen ◽  
Zhenghong Zhang ◽  
Jingjing Bi ◽  
Renfeng Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Corpus Luteum ◽  
Cell Apoptosis ◽  
In Vitro Study ◽  
Luteal Cell ◽  
Independent Manner ◽  
Luteal Regression ◽  
Luteal Cells

The increase of oxidative stress is one of the important characteristics of mammalian luteal regression. Previous investigations have revealed the essential role of reactive oxygen species (ROS) in luteal cell death during luteolysis, while it is unknown how ROS is regulated in this process. Considering the decrease of blood flow and increase of PGF2α during luteolysis, we hypothesized that the HIF-1α pathway may be involved in the regulation of ROS in the luteal cell of the late corpus luteum (CL). Here, by using a pseudopregnant rat model, we showed that the level of both HIF-1α and its downstream BNIP3 was increased during luteal regression. Consistently, we observed the increase of autophagy level during luteolysis, which is regulated in a Beclin1-independent manner. Comparing with early (Day 7 of pseudopregnancy) and middle CL (Day 14), the level of ROS was significantly increased in late CL, indicating the contribution of oxidative stress in luteolysis. Inhibition of HIF-1α by echinomycin (Ech), a potent HIF-1α inhibitor, ameliorated the upregulation of BNIP3 and NIX, as well as the induction of autophagy and the accumulation of ROS in luteal cells on Day 21 of pseudopregnancy. Morphologically, Ech treatment delayed the atrophy of the luteal structure at the late-luteal stage. An in vitro study indicated that inhibition of HIF-1α can also attenuate PGF2α-induced ROS and luteal cell apoptosis. Furthermore, the decrease of cell apoptosis can also be observed by ROS inhibition under PGF2α treatment. Taken together, our results indicated that HIF-1α signaling is involved in the regression of CL by modulating ROS production via orchestrating autophagy. Inhibition of HIF-1α could obviously hamper the apoptosis of luteal cells and the process of luteal regression.

scholarly journals Serum Fetuin-B Levels Are Elevated in Women with Metabolic Syndrome and Associated with Increased Oxidative Stress

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Shiyao Xue ◽  
Hongdong Han ◽  
Shunli Rui ◽  
Mengliu Yang ◽  
Yizhou Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Healthy Subjects ◽  
Bioinformatics Analysis ◽  
Cholesterol Metabolism ◽  
In Vitro Study ◽  
Multivariate Regression Analysis ◽  
Regulatory Factors ◽  
Triglyceride Content

Previous studies on serum fetuin-B (fetuin-like protein IRL685) have investigated its association with T2DM; however, the reason for the variation in serum fetuin-B and its regulatory factors in metabolic disease remain unclear. Here, we evaluated serum fetuin-B levels in women with newly diagnosed MetS and performed multiple interventions to investigate the role of fetuin-B in the pathogenesis of MetS. Serum fetuin-B levels were assessed using ELISA. Bioinformatics analysis was performed to analyze fetuin-B-related genes and signaling pathways. Additionally, oxidative stress parameters were measured in the in vitro study. For subgroup analyses, we performed EHC, OGTT, and treatment with a GLP-1RA to investigate the regulatory factors of serum fetuin-B. We found that in comparison with healthy subjects, serum fetuin-B levels were markedly increased in women with MetS. Further, serum fetuin-B showed a positive correlation with WHR, FAT%, TG, FBG, HbA1c, FIns, HOMA-IR, VAI, and LAP. Bioinformatics analysis revealed that most fetuin-B-related core genes were involved in cholesterol metabolism and fat decomposition. Consistent with this finding, multivariate regression analysis showed that triglyceride content and WHR were independently associated with serum fetuin-B. We also observed that serum fetuin-B levels were markedly elevated in healthy subjects after glucose loading and in women with MetS during EHC. In vitro, overexpression of fetuin-B promoted oxidative stress in HepG2 cell. After 6 months of treatment with a GLP-1RA, serum fetuin-B levels in women with MetS decreased following an improvement in metabolism and insulin sensitivity. Therefore, serum fetuin-B is associated with MetS, which may serve as a biomarker of oxidative stress. This trial is registered with ChiCTR-OCC-11001422.

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