scholarly journals Expression, activation, and role of AKT isoforms in the uterus

Reproduction ◽  
2014 ◽  
Vol 148 (5) ◽  
pp. R85-R95 ◽  
Author(s):  
François Fabi ◽  
Eric Asselin
Keyword(s):  
Cell Death ◽  
Endometrial Cancer ◽  
Embryo Implantation ◽  
Physiological Role ◽  
Molecular Processes ◽  
Cellular Processes ◽  
Akt Isoforms ◽  
High Level ◽  
Reproductive Processes

The three isoforms of AKT: AKT1, AKT2, and AKT3, are crucial regulators of both normal and pathological cellular processes. Each of these isoforms exhibits a high level of homology and functional redundancy with each other. However, while being highly similar and structurally homologous, a rising amount of evidence is showing that each isoform possesses specific targets as well as preferential subcellular localization. The role of AKT has been studied extensively in reproductive processes, but isoform-specific roles are yet to be fully understood. This review will focus on the role of AKT in the uterus and its function in processes related to cell death and proliferation such as embryo implantation, decidualization, endometriosis, and endometrial cancer in an isoform-centric manner. In this review, we will cover the activation of AKT in various settings, localization of isoforms in subcellular compartments, and the effect of isoform expression on cellular processes. To fully understand the dynamic molecular processes taking place in the uterus, it is crucial that we better understand the physiological role of AKT isoforms as well as their function in the emergence of diseases.

Mechanisms and regulations of endometrial angiogenesis

2002 ◽  
Vol 10 (1) ◽  
pp. 45-61 ◽  
Author(s):  
C Gargett ◽  
G Weston ◽  
PAW Rogers
Keyword(s):  
Endometrial Cancer ◽  
Menstrual Cycle ◽  
Corpus Luteum ◽  
Blood Vessels ◽  
Rapid Growth ◽  
Embryo Implantation ◽  
Breakthrough Bleeding ◽  
Reproductive Life ◽  
Reproductive Processes

Angiogenesis is defined as the formation of new blood vessels from the existing vasculature. Angiogenesis occurs regularly in the endometrium throughout the reproductive life of females as part of the rapid growth and regression of this tissue that occurs during the menstrual cycle. It is now clearly evident that angiogenesis plays a key role in reproductive processes such as embryo implantation, placentation, endometrial regeneration after menstruation, and in the ovary during folliculogenesis and corpus luteum formation. Given the complexity and continual change of the endometrial milieu, it seems highly likely that aberrations in the angiogenic process may contribute to various disorders, including endometrial cancer, endometriosis, menorrhagia and breakthrough bleeding – all significant and common gynaecological pathologies. This review provides an update on the mechanisms and regulation of endometrial angiogenesis, with particular reference to the role of angiogenesis in implantation and placentation, as well as two endometrial pathologies – endometriosis and breakthrough bleeding.

scholarly journals Caspase-14—From Biomolecular Basics to Clinical Approach. A Review of Available Data

2021 ◽  
Vol 22 (11) ◽  
pp. 5575
Author(s):  
Agnieszka Markiewicz ◽  
Dawid Sigorski ◽  
Mateusz Markiewicz ◽  
Agnieszka Owczarczyk-Saczonek ◽  
Waldemar Placek
Keyword(s):  
Cell Death ◽  
Physiological Role ◽  
Skin Barrier ◽  
Clinical Aspects ◽  
Clinical Approach ◽  
Search Term ◽  
Caspase Family ◽  
Skin Conditions ◽  
Theoretical Science

Caspase-14 is a unique member of the caspase family—a family of molecules participating in apoptosis. However, it does not affect this process but regulates another form of programmed cell death—cornification, which is characteristic of the epidermis. Therefore, it plays a crucial role in the formation of the skin barrier. The cell death cycle has been a subject of interest for researchers for decades, so a lot of research has been done to expand the understanding of caspase-14, its role in cell homeostasis and processes affecting its expression and activation. Conversely, it is also an interesting target for clinical researchers searching for its role in the physiology of healthy individuals and its pathophysiology in particular diseases. A summary was done in 2008 by Denecker et al., concentrating mostly on the biotechnological aspects of the molecule and its physiological role. However, a lot of new data have been reported, and some more practical and clinical research has been conducted since then. The majority of studies tackled the issue of clinical data presenting the role of caspase in the etiopathology of many diseases such as retinal dysfunctions, multiple malignancies, and skin conditions. This review summarizes the available knowledge on the molecular and, more interestingly, the clinical aspects of caspase-14. It also presents how theoretical science may pave the way for medical research. Methods: The authors analyzed publications available on PubMed until 21 March 2021, using the search term “caspase 14”.

scholarly journals Interphotoreceptor coupling: an evolutionary perspective

2021 ◽  
Author(s):  
Lorenzo Cangiano ◽  
Sabrina Asteriti
Keyword(s):  
Visual Information ◽  
Signal To Noise Ratio ◽  
Electrical Coupling ◽  
Physiological Role ◽  
Cellular Processes ◽  
Contact Points ◽  
Highly Sensitive ◽  
The Many ◽  
The Impact

AbstractIn the vertebrate retina, signals generated by cones of different spectral preference and by highly sensitive rod photoreceptors interact at various levels to extract salient visual information. The first opportunity for such interaction is offered by electrical coupling of the photoreceptors themselves, which is mediated by gap junctions located at the contact points of specialised cellular processes: synaptic terminals, telodendria and radial fins. Here, we examine the evolutionary pressures for and against interphotoreceptor coupling, which are likely to have shaped how coupling is deployed in different species. The impact of coupling on signal to noise ratio, spatial acuity, contrast sensitivity, absolute and increment threshold, retinal signal flow and colour discrimination is discussed while emphasising available data from a variety of vertebrate models spanning from lampreys to primates. We highlight the many gaps in our knowledge, persisting discrepancies in the literature, as well as some major unanswered questions on the actual extent and physiological role of cone-cone, rod-cone and rod-rod communication. Lastly, we point toward limited but intriguing evidence suggestive of the ancestral form of coupling among ciliary photoreceptors.

Structure, Function, Involvement in Diseases and Targeting of 14-3-3 Proteins: An Update

2018 ◽  
Vol 25 (1) ◽  
pp. 5-21 ◽  
Author(s):  
Ylenia Cau ◽  
Daniela Valensin ◽  
Mattia Mori ◽  
Sara Draghi ◽  
Maurizio Botta
Keyword(s):  
Protein Interactions ◽  
Molecular Mechanisms ◽  
Physiological Role ◽  
Specific Protein ◽  
Protein Protein Interactions ◽  
Cellular Processes ◽  
Protein Partners ◽  
High Sequence Homology ◽  
Small Molecule Modulators

14-3-3 is a class of proteins able to interact with a multitude of targets by establishing protein-protein interactions (PPIs). They are usually found in all eukaryotes with a conserved secondary structure and high sequence homology among species. 14-3-3 proteins are involved in many physiological and pathological cellular processes either by triggering or interfering with the activity of specific protein partners. In the last years, the scientific community has collected many evidences on the role played by seven human 14-3-3 isoforms in cancer or neurodegenerative diseases. Indeed, these proteins regulate the molecular mechanisms associated to these diseases by interacting with (i) oncogenic and (ii) pro-apoptotic proteins and (iii) with proteins involved in Parkinson and Alzheimer diseases. The discovery of small molecule modulators of 14-3-3 PPIs could facilitate complete understanding of the physiological role of these proteins, and might offer valuable therapeutic approaches for these critical pathological states.

scholarly journals Bub1 mediates cell death in response to chromosome missegregation and acts to suppress spontaneous tumorigenesis

2007 ◽  
Vol 179 (2) ◽  
pp. 255-267 ◽  
Author(s):  
Karthik Jeganathan ◽  
Liviu Malureanu ◽  
Darren J. Baker ◽  
Susan C. Abraham ◽  
Jan M. van Deursen
Keyword(s):  
Cell Death ◽  
Chromosome Segregation ◽  
Physiological Role ◽  
Mitotic Checkpoint ◽  
Critical Threshold ◽  
Wild Type ◽  
Checkpoint Protein ◽  
Chromosome Missegregation ◽  
Mitotic Checkpoint Protein

The physiological role of the mitotic checkpoint protein Bub1 is unknown. To study this role, we generated a series of mutant mice with a gradient of reduced Bub1 expression using wild-type, hypomorphic, and knockout alleles. Bub1 hypomorphic mice are viable, fertile, and overtly normal despite weakened mitotic checkpoint activity and high percentages of aneuploid cells. Bub1 haploinsufficient mice, which have a milder reduction in Bub1 protein than Bub1 hypomorphic mice, also exhibit reduced checkpoint activity and increased aneuploidy, but to a lesser extent. Although cells from Bub1 hypomorphic and haploinsufficient mice have similar rates of chromosome missegregation, cell death after an aberrant separation decreases dramatically with declining Bub1 levels. Importantly, Bub1 hypomorphic mice are highly susceptible to spontaneous tumors, whereas Bub1 haploinsufficient mice are not. These findings demonstrate that loss of Bub1 below a critical threshold drives spontaneous tumorigenesis and suggest that in addition to ensuring proper chromosome segregation, Bub1 is important for mediating cell death when chromosomes missegregate.

The role of hypoxia in endometrial cancer

2021 ◽  
Vol 22 ◽  
Author(s):  
Yarely M. Salinas-Vera ◽  
Dolores Gallardo-Rincón ◽  
Erika Ruíz-García ◽  
Macrina B. Silva-Cázares ◽  
Carmen Sol de la Peña-Cruz ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Targeted Therapies ◽  
Current Knowledge ◽  
Vasculogenic Mimicry ◽  
Cellular Processes ◽  
Corpus Uteri

: Endometrial cancer represents the most frequent neoplasia from the corpus uteri, and comprises the 14th leading cause of death in women worldwide. Risk factors that contribute to the disease include early menarche, late menopause, nulliparity, and menopausal hormone use, as well as hypertension and obesity comorbidities. The clinical effectiveness of chemotherapy is variable, suggesting that novel molecular targeted therapies against specific cellular processes associated with the maintenance of cancer cell survival and therapy resistance urged to ameliorate the rates of success in endometrial cancer treatment. In the course of tumor growth, cancer cells must adapt to decreased oxygen availability in the microenvironment by upregulation of hypoxia-inducible factors, which orchestrate the activation of a transcriptional program leading to cell survival. During this adaptative process, the hypoxic cancer cells may acquire invasive and metastatic properties as well as increased cell proliferation and resistance to chemotherapy, enhanced angiogenesis, vasculogenic mimicry, and maintenance of cancer cell stemness, which contribute to more aggressive cancer phenotypes. Several studies have shown that hypoxia-inducible factor 1 alpha (HIF-1α) protein is aberrantly overexpressed in many solid tumors from breast, prostate, ovarian, bladder, colon, brain, and pancreas. Thus, it has been considered an important therapeutic target. Here, we reviewed the current knowledge of the relevant roles of cellular hypoxia mechanisms and HIF-1α functions in diverse processes associated with endometrial cancer progression. In addition, we also summarize the role of microRNAs in the posttranscriptional regulation of protein-encoding genes involved in the hypoxia response in endometrial cancer. Finally, we pointed out the need for urgent targeted therapies to impair the cellular processes activated by hypoxia in the tumor microenvironment.

SUBSTANTIATION OF NECESSITY OF APPLICATION OF PHOSPHOLIPIDS IN THE PRODUCTION OF FUNCTIONAL FOODSTUFFS

2018 ◽  
Author(s):  
Н.Н. КОРНЕН ◽  
С.А. КАЛМАНОВИЧ ◽  
Т.А. ШАХРАЙ ◽  
Е.П. ВИКТОРОВА
Keyword(s):  
Nutritional Status ◽  
Dietary Supplements ◽  
Physiological Role ◽  
Regulatory Function ◽  
Medical Sciences ◽  
Cellular Processes ◽  
Level Of Knowledge ◽  
Protective Fabrics ◽  
Technological University

Проведен анализ современных научных представлений о роли фосфолипидов (ФЛ) в обеспечении функционирования биомембран и их регуляторной функции в важнейших клеточных процессах. Из ФЛ состоит 50% печени, 1/3 мозговых изолирующих и защитных тканей, окружающих головной и спинной мозг. По рекомендациям РАМН, физиологическая потребность взрослого человека в ФЛ составляет 5–7 г/сут. Согласно проведенным исследованиям, в пищевом статусе населения РФ дефицит ФЛ составляет от 50 до 80%. Показано, что современный уровень знаний о физиологической роли ФЛ способствует созданию и внедрению в производство фосфолипидных продуктов на основе ФЛ и фосфолипидных БАД на основе растительных лецитинов, употребление которых может нормализовать пищевой статус. Дано описание фосфолипидных продуктов и БАД серии Тонус (Супер-Тонус, Фито-Тонус, Тонус-Плюс) и серии Витол (Витол, Витол-Холин и Витол-ФЭИ), разработанных учеными Кубанского государственного технологического университета. Показаны возможности применения растительных лецитинов, фосфолипидных продуктов и БАД на их основе в качестве многофункциональных рецептурных компонентов при производстве пищевых продуктов функционального и специализированного назначения. The analysis of modern scientific ideas about the role of phospholipids (FL) in ensuring the functioning of biomembranes and their regulatory function in the most important cellular processes is carried out. So, 50% of a liver, 1/3 brain isolating and protective fabrics surrounding a brain and spinal cord consist of FL. According to the recommendations of the Russian Academy of Medical Sciences, the physiological need of an adult in FL is 5–7 g/day. According to the conducted studies, in the nutritional status of the Russian population, the deficit of FL is from 50 to 80%. It is shown that the current level of knowledge about the physiological role of FL contributes to the creation and introduction of phospholipid products based on FL and phospholipid supplements on the basis of vegetable lecithins, the use of which can normalize the nutritional status. The description of phospholipid products and dietary supplements developed by scientists of the Kuban State Technological University of the Tonus series (Super Tonus, Phyto Tonus, Tonus Plus) and the Vitol series (Vitol, Vitol Kholin and Vitol FEI) is given. The possibilities of using vegetable lecithins, phospholipid products and dietary supplements on their basis are shown as multifunctional prescription components in the production of functional and specialized food products.

scholarly journals A control engineering approach to understanding the TGF-β paradox in cancer

2011 ◽  
Vol 9 (71) ◽  
pp. 1389-1397 ◽  
Author(s):  
Seung-Wook Chung ◽  
Carlton R. Cooper ◽  
Mary C. Farach-Carson ◽  
Babatunde A. Ogunnaike
Keyword(s):  
Cancer Cells ◽  
Mechanistic Model ◽  
Tumour Suppressor ◽  
Cancer Tissue ◽  
Control Engineering ◽  
Cellular Processes ◽  
Proliferation And Apoptosis ◽  
High Level ◽  
Quantitative Explanation

TGF-β, a key cytokine that regulates diverse cellular processes, including proliferation and apoptosis, appears to function paradoxically as a tumour suppressor in normal cells, and as a tumour promoter in cancer cells, but the mechanisms underlying such contradictory roles remain unknown. In particular, given that this cytokine is primarily a tumour suppressor, the conundrum of the unusually high level of TGF-β observed in the primary cancer tissue and blood samples of cancer patients with the worst prognosis, remains unresolved. To provide a quantitative explanation of these paradoxical observations, we present, from a control theory perspective, a mechanistic model of TGF-β-driven regulation of cell homeostasis. Analysis of the overall system model yields quantitative insight into how cell population is regulated, enabling us to propose a plausible explanation for the paradox: with the tumour suppressor role of TGF-β unchanged from normal to cancer cells, we demonstrate that the observed increased level of TGF-β is an effect of cancer cell phenotypic progression (specifically, acquired TGF-β resistance), not the cause . We are thus able to explain precisely why the clinically observed correlation between elevated TGF-β levels and poor prognosis is in fact consistent with TGF-β's original (and unchanged) role as a tumour suppressor.

scholarly journals Non-Coding RNAs in Endometrial Physiopathology

2018 ◽  
Vol 19 (7) ◽  
pp. 2120 ◽  
Author(s):  
Alessandro La Ferlita ◽  
Rosalia Battaglia ◽  
Francesca Andronico ◽  
Salvatore Caruso ◽  
Antonio Cianci ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Human Genome ◽  
Human Genome Project ◽  
Embryo Implantation ◽  
Genome Project ◽  
Rna Molecules ◽  
Cellular Processes ◽  
Non Coding Rnas ◽  
The Human Genome Project ◽  
Heterogeneous Class

The Human Genome Project led to the discovery that about 80% of our DNA is transcribed in RNA molecules. Only 2% of the human genome is translated into proteins, the rest mostly produces molecules called non-coding RNAs, which are a heterogeneous class of RNAs involved in different steps of gene regulation. They have been classified, according to their length, into small non-coding RNAs and long non-coding RNAs, or to their function, into housekeeping non-coding RNAs and regulatory non-coding RNAs. Their involvement has been widely demonstrated in all cellular processes, as well as their dysregulation in human pathologies. In this review, we discuss the function of non-coding RNAs in endometrial physiology, analysing their involvement in embryo implantation. Moreover, we explore their role in endometrial pathologies such as endometrial cancer, endometriosis and chronic endometritis.

scholarly journals Expression of a Mitochondrial Peroxiredoxin Prevents Programmed Cell Death in Leishmania donovani

2006 ◽  
Vol 5 (5) ◽  
pp. 861-870 ◽  
Author(s):  
Simone Harder ◽  
Meike Bente ◽  
Kerstin Isermann ◽  
Iris Bruchhaus
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Mitochondrial Membrane ◽  
Leishmania Donovani ◽  
Physiological Role ◽  
Logarithmic Phase ◽  
Insect Vector ◽  
Oxygen Species ◽  
Late Logarithmic Phase

ABSTRACT Leishmania promastigote cells transmitted by the insect vector get phagocytosed by macrophages and convert into the amastigote form. During development and transformation, the parasites are exposed to various concentrations of reactive oxygen species, which can induce programmed cell death (PCD). We show that a mitochondrial peroxiredoxin (LdmPrx) protects Leishmania donovani from PCD. Whereas this peroxiredoxin is restricted to the kinetoplast area in promastigotes, it covers the entire mitochondrion in amastigotes, accompanied by dramatically increased expression. A similar change in the expression pattern was observed during the growth of Leishmania from the early to the late logarithmic phase. Recombinant LdmPrx shows typical peroxiredoxin-like enzyme activity. It is able to detoxify organic and inorganic peroxides and prevents DNA from hydroxyl radical-induced damage. Most notably, Leishmania parasites overexpressing this peroxiredoxin are protected from hydrogen peroxide-induced PCD. This protection is also seen in promastigotes grown to the late logarithmic phase, also characterized by high expression of this peroxiredoxin. Apparently, the physiological role of this peroxiredoxin is stabilization of the mitochondrial membrane potential and, as a consequence, inhibition of PCD through removal of peroxides.

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