scholarly journals The Role of Oxidative Stress and Membrane Transport Systems during Endometriosis: A Fresh Look at a Busy Corner

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Salvatore Giovanni Vitale ◽  
Stella Capriglione ◽  
Isabel Peterlunger ◽  
Valentina Lucia La Rosa ◽  
Amerigo Vitagliano ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Disease Onset ◽  
Uterine Cavity ◽  
Transport Systems ◽  
Female Population ◽  
Endometrial Cells ◽  
Cytokines And Chemokines ◽  
Chronic Inflammatory Reaction ◽  
Membrane Transport Systems

Endometriosis is a condition characterized by the presence of endometrial tissue outside the uterine cavity, leading to a chronic inflammatory reaction. It is one of the most widespread gynecological diseases with a 10–15% prevalence in the general female population, rising up to 30–45% in patients with infertility. Although it was first described in 1860, its etiology and pathogenesis are still unclear. It is now accepted that inflammation plays a central role in the development and progression of endometriosis. In particular, it is marked by an inflammatory process associated with the overproduction of an array of inflammatory mediators such as prostaglandins, metalloproteinases, cytokines, and chemokines. In addition, the growth and adhesion of endometrial cells in the peritoneal cavity due to reactive oxygen species (ROS) and free radicals lead to disease onset, its ensuing symptoms—among which pain and infertility. The aim of our review is to evaluate the role of oxidative stress and ROS in the pathogenesis of endometriosis and the efficacy of antioxidant therapy in the treatment and mitigation of its symptoms.

scholarly journals Estrogen- and Progesterone (P4)-Mediated Epigenetic Modifications of Endometrial Stromal Cells (EnSCs) and/or Mesenchymal Stem/Stromal Cells (MSCs) in the Etiopathogenesis of Endometriosis

2021 ◽  
Author(s):  
Dariusz Szukiewicz ◽  
Aleksandra Stangret ◽  
Carmen Ruiz-Ruiz ◽  
Enrique G. Olivares ◽  
Olga Soriţău ◽  
...  
Keyword(s):  
Stromal Cells ◽  
Uterine Cavity ◽  
Retrograde Transport ◽  
Surrounding Tissue ◽  
Pelvic Cavity ◽  
Endometrial Stromal Cells ◽  
Endometrial Cells ◽  
Estrogen Exposure ◽  
Chronic Inflammatory Condition

AbstractEndometriosis is a common chronic inflammatory condition in which endometrial tissue appears outside the uterine cavity. Because ectopic endometriosis cells express both estrogen and progesterone (P4) receptors, they grow and undergo cyclic proliferation and breakdown similar to the endometrium. This debilitating gynecological disease affects up to 15% of reproductive aged women. Despite many years of research, the etiopathogenesis of endometrial lesions remains unclear. Retrograde transport of the viable menstrual endometrial cells with retained ability for attachment within the pelvic cavity, proliferation, differentiation and subsequent invasion into the surrounding tissue constitutes the rationale for widely accepted implantation theory. Accordingly, the most abundant cells in the endometrium are endometrial stromal cells (EnSCs). These cells constitute a particular population with clonogenic activity that resembles properties of mesenchymal stem/stromal cells (MSCs). Thus, a significant role of stem cell-based dysfunction in formation of the initial endometrial lesions is suspected. There is increasing evidence that the role of epigenetic mechanisms and processes in endometriosis have been underestimated. The importance of excess estrogen exposure and P4 resistance in epigenetic homeostasis failure in the endometrial/endometriotic tissue are crucial. Epigenetic alterations regarding transcription factors of estrogen and P4 signaling pathways in MSCs are robust in endometriotic tissue. Thus, perspectives for the future may include MSCs and EnSCs as the targets of epigenetic therapies in the prevention and treatment of endometriosis. Here, we reviewed the current known changes in the epigenetic background of EnSCs and MSCs due to estrogen/P4 imbalances in the context of etiopathogenesis of endometriosis.

The scattered puzzle effect: implantation disorders in chronic endometritis

GYNECOLOGY ◽  
2020 ◽  
Vol 22 (6) ◽  
pp. 93-100
Author(s):  
Victor E. Radzinsky ◽  
Mekan R. Orazov ◽  
Liliia R. Toktar ◽  
Liudmila M. Mihaleva ◽  
Pavel A. Semenov ◽  
...  
Keyword(s):  
Uterine Cavity ◽  
Special Role ◽  
Inadequate Response ◽  
Chronic Endometritis ◽  
Vitro Fertilization ◽  
Endometrial Cells ◽  
Adverse Pregnancy ◽  
Relationship Of

Chronic endometritis (CE) is defined as a state of inflammation localized in the endometrium, accompanied by edema, dissociated maturation of epithelial cells and fibroblasts, increased stromal density and the presence of plasma cell infiltrate in it. The connection between chronic inflammation in the endometrium and infertility deserves special attention. Inadequate response of immunocompetent endometrial cells, including impaired synthesis of proinflammatory cytokines, dysreceptiveness, disorders of proliferation and differentiation processes are the main links in the formation of infertility in patients with CE. Despite the fact that the presence of a normocenosis of the uterine cavity today is not in doubt this is a physiological norm, persistent bacterial infection of the endometrium is still called the main etiopathogenetic factor of CE and, therefore, the main point of application of therapeutic agents. Nevertheless, a number of works have emphasized the special role of not bacterial, but viral etiology of endometritis, especially in the context of infertility developing against this background. It seems that the role of viral endometrial infection in adverse pregnancy outcomes and in vitro fertilization programs is underestimated. Further research is needed to clarify the relationship of viral infection as a trigger of implantation failure in infertile women with CE.

scholarly journals Curcumin and Endometriosis

2020 ◽  
Vol 21 (7) ◽  
pp. 2440 ◽  
Author(s):  
Alexandre Vallée ◽  
Yves Lecarpentier
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Uterine Cavity ◽  
Main Role ◽  
Oxygen Species ◽  
Inflammatory Agent ◽  
Gynecological Disorders ◽  
Anti Oxidant ◽  
Anti Inflammatory

Endometriosis is one of the main common gynecological disorders, which is characterized by the presence of glands and stroma outside the uterine cavity. Some findings have highlighted the main role of inflammation in endometriosis by acting on proliferation, apoptosis and angiogenesis. Oxidative stress, an imbalance between reactive oxygen species and antioxidants, could have a key role in the initiation and progression of endometriosis by resulting in inflammatory responses in the peritoneal cavity. Nevertheless, the mechanisms underlying this disease are still unclear and therapies are not currently efficient. Curcumin is a major anti-inflammatory agent. Several findings have highlighted the anti-oxidant, anti-inflammatory and anti-angiogenic properties of curcumin. The purpose of this review is to summarize the potential action of curcumin in endometriosis by acting on inflammation, oxidative stress, invasion and adhesion, apoptosis and angiogenesis.

Oxygen-sensitive membrane transporters in vertebrate red cells

2000 ◽  
Vol 203 (9) ◽  
pp. 1395-1407 ◽  
Author(s):  
J.S. Gibson ◽  
A.R. Cossins ◽  
J.C. Ellory
Keyword(s):  
Membrane Transporters ◽  
Red Cells ◽  
Transport Systems ◽  
Red Cell ◽  
Organic Systems ◽  
Wide Range ◽  
Oxygen Sensitive ◽  
Radical Generation ◽  
Membrane Transport Systems

Oxygen is essential for all higher forms of animal life. It is required for oxidative phosphorylation, which forms the bulk of the energy supply of most animals. In many vertebrates, transport of O(2) from respiratory to other tissues, and of CO(2) in the opposite direction, involves red cells. These are highly specialised, adapted for their respiratory function. Intracellular haemoglobin, carbonic anhydrase and the membrane anion exchanger (AE1) increase the effective O(2)- and CO(2)-carrying capacity of red cells by approximately 100-fold. O(2) also has a pathological role. It is a very reactive species chemically, and oxidation, free radical generation and peroxide formation can be major hazards. Cells that come into contact with potentially damaging levels of O(2) have a variety of systems to protect them against oxidative damage. Those in red cells include catalase, superoxide dismutase and glutathione. In this review, we focus on a third role of O(2), as a regulator of membrane transport systems, a role with important consequences for the homeostasis of the red cell and also the organism as a whole. We show that regulation of red cell transporters by O(2) is widespread throughout the vertebrate kingdom. The effect of O(2) is selective but involves a wide range of transporters, including inorganic and organic systems, and both electroneutral and conductive pathways. Finally, we discuss what is known about the mechanism of the O(2) effect and comment on its physiological and pathological roles.

scholarly journals Interplay between Manganese and Iron in Pneumococcal Pathogenesis: Role of the Orphan Response Regulator RitR

2012 ◽  
Vol 81 (2) ◽  
pp. 421-429 ◽  
Author(s):  
Cheryl-Lynn Y. Ong ◽  
Adam J. Potter ◽  
Claudia Trappetti ◽  
Mark J. Walker ◽  
Michael P. Jennings ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Iron Uptake ◽  
Metal Ion ◽  
Response Regulator ◽  
Transport Systems ◽  
Bacterial Cells ◽  
Content Type ◽  
Manganese Ion ◽  
Iron And Manganese

ABSTRACTStreptococcus pneumoniae(the pneumococcus) is a major human pathogen that is carried asymptomatically in the nasopharynx by up to 70% of the human population. Translocation of the bacteria into internal sites can cause a range of diseases, such as pneumonia, otitis media, meningitis, and bacteremia. This transition from nasopharynx to growth at systemic sites means that the pneumococcus needs to adjust to a variety of environmental conditions, including transition metal ion availability. Although it is an important nutrient, iron potentiates oxidative stress, and it is established that inS. pneumoniae, expression of iron transport systems and proteins that protect against oxidative stress are regulated by an orphan response regulator, RitR. In this study, we investigated the effect of iron and manganese ion availability on the growth of aritRmutant. Deletion ofritRled to impaired growth of bacteria in high-iron medium, but this phenotype could be suppressed with the addition of manganese. Measurement of metal ion accumulation indicated that manganese prevents iron accumulation. Furthermore, the addition of manganese also led to a reduction in the amount of hydrogen peroxide produced by bacterial cells. Studies of virulence in a murine model of infection indicated that RitR was not essential for pneumococcal survival and suggested that derepression of iron uptake systems may enhance the survival of pneumococci in some niches.

scholarly journals ENDOMETRIOSIS AND OXIDATIVE-ANTIOXIDATIVE IMBALANCE STATUS. THE ROLE OF FLAVONOIDS, CURCUMIN AND N-ACETYLCYSTEINE

InterConf ◽  
2021 ◽  
pp. 477-483
Author(s):  
Monika Ruszała ◽  
Dominik Dłuski ◽  
Aneta Zamojska ◽  
Agnieszka Wańkowicz ◽  
Marek Gogacz
Keyword(s):  
Reactive Oxygen Species ◽  
Unpaired Electron ◽  
Uterine Cavity ◽  
Reactive Oxygen ◽  
Reproductive Age ◽  
Oxygen Species ◽  
Cytokines And Chemokines ◽  
The World ◽  
Immunological Factors

Endometriosis is a silent, unseen and painful female illness which is characterized by the presence of glands and stroma outside the uterine cavity. Approximately one in ten women in a reproductive age around the world suffer from endometriosis of whom nearly half is treated due to infertility. The pathogenesis and mechanisms that determines the occurence of the disease are still unknown. Immunological factors have been observed in the initiation and development of endometriosis. An imbalance between reactive oxygen species (molecules having an unpaired electron) and antioxidants leads to the upregulation of metalloproteinases, prostaglandins, cytokines and chemokines.

scholarly journals Oxidative Stress and Membrane Transport Systems

2018 ◽  
Vol 2018 ◽  
pp. 1-2
Author(s):  
Angela Marino ◽  
Silvia Dossena ◽  
Grazia Tamma ◽  
Sandra Donnini
Keyword(s):  
Oxidative Stress ◽  
Membrane Transport ◽  
Transport Systems ◽  
Membrane Transport Systems

scholarly journals Disruption of F-actin stimulates hypertonic activation of the BGT1 transporter in MDCK cells

2003 ◽  
Vol 284 (5) ◽  
pp. F930-F937 ◽  
Author(s):  
Jeremy L. Bricker ◽  
Shaoyou Chu ◽  
Stephen A. Kempson
Keyword(s):  
Actin Cytoskeleton ◽  
Mdck Cells ◽  
Major Change ◽  
Cytochalasin D ◽  
Transport Systems ◽  
Microtubule Network ◽  
Cell Monolayers ◽  
Latrunculin A ◽  
Membrane Transport Systems

Many membrane transport systems are altered by changes in the state of the actin cytoskeleton. Although an intact microtubule network is required for hypertonic activation of the betaine transporter (BGT1), the possible role of the actin cytoskeleton is unknown. BGT1 function in Madin-Darby canine kidney cell monolayers was assessed as Na+-dependent uptake of GABA, following disassembly of F-actin by cytochalasin D (1.0 μM) or latrunculin A (0.6 μM). Both drugs significantly increased ( P < 0.001) the activation of BGT1 transport by 24-h hypertonicity (500 mosmol/kgH2O). In contrast, the hypertonic upregulation of Na+-dependent alanine uptake remained unaltered by cytochalasin D. Disruption of F-actin did not interfere with downregulation of BGT1 transport when cells were transferred from hypertonic to isotonic medium. Immunofluorescence staining revealed colocalization of BGT1 and F-actin at the plasma membrane of hypertonic cells. Surface biotinylation revealed no major change in BGT1 protein abundance after cytochalasin D action, suggesting that stimulation of hypertonic activation of BGT1 transport is due to increased activity of existing BGT1 transporters.

scholarly journals Role of thyroid dysimmunity and thyroid hormones in endometriosis

2019 ◽  
pp. 201820469
Author(s):  
Marine Peyneau ◽  
Niloufar Kavian ◽  
Sandrine Chouzenoux ◽  
Carole Nicco ◽  
Mohamed Jeljeli ◽  
...  
Keyword(s):  
Thyroid Hormones ◽  
Thyroid Autoimmunity ◽  
Uterine Cavity ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Disorder ◽  
Endometrial Cells ◽  
Thyroid Metabolism ◽  
Ectopic Endometrium

Endometriosis is characterized by the presence of ectopic endometrial cells outside the uterine cavity. Thyroid autoimmunity has been associated with endometriosis. This work investigated the potential pathophysiological link between endometriosis and thyroid disorders. Transcripts and proteins involved in thyroid metabolism are dysregulated in eutopic and ectopic endometrium of endometriotic patients, leading to resistance of ectopic endometrium to triiodothyronine (T3) action and local accumulation of thyroxine (T4). Thyroid-stimulating hormone (TSH) acts as a proliferative and prooxidative hormone on all endometria of endometriosis patients and controls, whereas T3 and T4 act to specifically increase ectopic endometrial cell proliferation and reactive oxygen species (ROS) production. Mouse studies confirmed the data gained in vitro since endometriotic implants were found to be bigger when thyroid hormones increased. A retrospective analysis of endometriosis patients with or without a thyroid disorder revealed an increased chronic pelvic pain and disease score in endometriotic patients with a thyroid disorder.

scholarly journals Betulinic Acid Inhibits Endometriosis Through Suppression of Estrogen Receptor β Signaling Pathway

2020 ◽  
Vol 11 ◽  
Author(s):  
Dongfang Xiang ◽  
Min Zhao ◽  
Xiaofan Cai ◽  
Yongxia Wang ◽  
Lei Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Estrogen Receptor ◽  
Signaling Pathway ◽  
Betulinic Acid ◽  
Epigenetic Modification ◽  
Uterine Cavity ◽  
Tissue Growth ◽  
Estrogen Receptor Β ◽  
Endometrial Cells

Endometriosis is an inflammatory gynecological disorder characterized by endometrial tissue growth located outside of the uterine cavity in addition to chronic pelvic pain and infertility. In this study, we aim to develop a potential therapeutic treatment based on the pathogenesis and mechanism of Endometriosis. Our preliminary data showed that the expression of estrogen receptor β (ERβ) was significantly increased, while ERα was significantly decreased, in endometriotic cells compared to normal endometrial cells. Further investigation showed that betulinic acid (BA) treatment suppressed ERβ expression through epigenetic modification on the ERβ promoter, while had no effect on ERα expression. In addition, BA treatment suppresses ERβ target genes, including superoxide dismutase 2 (SOD2), nuclear respiratory factor-1 (NRF1), cyclooxygenase 2 (COX2), and matrix metalloproteinase-1 (MMP1), subsequently increasing oxidative stress, triggering mitochondrial dysfunction, decreasing elevated proinflammatory cytokines, and eventually suppressing endometriotic cell proliferation, mimicking the effect of ERβ knockdown. On the other hand, gain of ERβ by lentivirus infection in normal endometrial cells resulted in increased cell proliferation and proinflammatory cytokine release, while BA treatment diminished this effect through ERβ suppression with subsequent oxidative stress and apoptosis. Our results indicate that ERβ may be a major driving force for the development of endometriosis, while BA inhibits Endometriosis through specific suppression of the ERβ signaling pathway. This study provides a novel therapeutic strategy for endometriosis treatment through BA-mediated ERβ suppression.

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