Quantitative polymorphism of tandem repeats as a method of epigenetic regulation of the of human cells response to oxidative stress

2020 ◽  
pp. 68-70
Author(s):  
Н.Н. Вейко ◽  
Е.С. Ершова ◽  
М.С. Конькова ◽  
Е.М. Малиновская ◽  
С.В. Костюк
Keyword(s):  
Adaptive Response ◽  
Spatial Organization ◽  
Tandem Repeats ◽  
Spatial Configuration ◽  
Human Cells ◽  
Central Regions ◽  
Schizophrenic Patients ◽  
Response To Stress ◽  
Cell Genome ◽  
And Function

Пространственная организация хроматина важна для нормального функционирования клетки. На архитектуру ядра влияют размеры отдельных фрагментов генома, которые коррелируют с числом копий этих фрагментов. Перемещение локусов 1q12 от поверхности ядра в центральные области является ключевой стадией адаптивного ответа клетки на стресс. Мы предположили, что размер локусов 1q12, который коррелирует с содержанием повтора f-SatIII, может влиять на перемещение этих участков хроматина в ядре. Методом FISH на выделенных лимфоцитах показали, что в контроле локусы 1q12 расположены вблизи поверхности ядра, в ядрах лимфоцитов больных шизофренией (БШ) и облученных контрольных клеток локусы 1q12 расположены в центральных районах ядра. Длительное культивирование облученных лимфоцитов сопровождалось гибелью клеток, и снижением содержания f-SatIII в ДНК. Очевидно, что погибали клетки с большим размером 1q12 (много f-SatIII), обогащая популяцию клетками с низким содержанием f-SatIII. В клетках БШ и в облученных клетках мы обнаружили повышение уровня РНК SATIII. Размеры гетерохроматина 1q12 в клетках человека могут влиять на процессы пролиферации и ответа клетки на стресс. Количественный полиморфизм тандемных повторов генома - один из эпигенетических механизмов регуляции ответа клеток на окислительный стресс. The spatial organization of chromatin is important for the normal functioning of the cell. Genome repeat cluster sizes can affect the chromatin spatial configuration and function. The 1q12 heterochromatin loci movement from the periphery to the center of the nucleus is the cells’ universal response to various types of stress. We hypothesized that a large 1q12 domain could affect chromatin movement, thereby inhibiting adaptive response (AR). Using the FISH method, we shown that in the control, 1q12 loci are located near the surface of the nucleus; in the lymphocyte nuclei of schizophrenic patients and irradiated control cells, 1q12 loci are located in the central regions of the nucleus. During prolonged cultivation, the irradiated cells with a large Large f-SatIII amount die and the population is enriched with the cells with low f-SatIII content. In intact SZ patients’ lymphocytes and in irradiated cells we found an increase in SATIII RNA levels. The size of heterochromatin 1q12 loci in human cells can affect to the proliferation and cells’ adaptive response to stress. Quantitative polymorphism of tandem genome repeats is one of the epigenetic mechanisms of genome expression’s regulation.

scholarly journals Age and homeostasis

2020 ◽  
pp. 79-86
Author(s):  
А.А. Пальцын ◽  
Н.Б. Свиридкина
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Adaptive Response ◽  
Cold Shock ◽  
Structure And Function ◽  
The Body ◽  
Adequate Response ◽  
Response To Stress ◽  
And Function ◽  
Homeostatic Response

Гомеостаз - способность организма сохранять достаточное для жизни постоянство структуры и функции. Противоречие заключается в том, что суть жизни - это неизбежное изменение структуры и функции. Наиболее распространенный нарушитель гомеостаза - оксидативный стресс. В нейтрализации его действия участвует множество генов, включаемых транскрипционными факторами Nrf2, NFκB, TFAM, и PGC1α. Адаптивный ответ развивается не только на оксидативный стресс, но и на тепловой шок, гликемический стресс, холодовой шок, осмотический стресс, переутомление, голодание, механический стресс, антигенное воздействие, эмоциональный и психологический стресс. При стрессе в клетках накапливаются продукты неполного протеолиза - агрегаты. Гомеостатический ответ выражается увеличением содержания шаперонов, способствующих правильному свертыванию белков и протеасом, разрушающих агрегаты. Однако способность адекватно отвечать на стрессы снижается с возрастом, сужается диапазон модулирования адаптивного гомеостаза. Нарастает вероятность выхода за пределы сузившегося диапазона и гибели клетки. Homeostasis is the ability of the body to maintain sufficient for life permanence of structure and function. A contradiction is that the essence of life is inevitable changes in the structure and function. The most common homeostasis violator is oxidative stress. Numerous genes triggered by Nrf2, NFκB, TFAM, and PGC1α transcription factors are involved in neutralizing the action of oxidative stress. The adaptive response is induced not only by oxidative stress but also by heat shock, glycemic stress, cold shock, osmotic stress, exhastion, starvation, mechanical stress, antigenic impact, and emotional or psychological stress. In stress, cells accumulate products of incomplete proteolysis, aggregates. The homeostatic response is evident as increased content of chaperones that contribute to the proper folding of proteins, and proteasomes that destroy the aggregates. However, the capability for an adequate response to stress declines with age, and the range of adaptive homeostasis modulation narrows. The probability of going beyond this narrowed range and of cell death is increasing.

scholarly journals Stimulation of proliferation, differentiation, and function of human cells by primate interleukin 3.

1987 ◽  
Vol 84 (9) ◽  
pp. 2761-2765 ◽  
Author(s):  
A. F. Lopez ◽  
L. B. To ◽  
Y. C. Yang ◽  
J. R. Gamble ◽  
M. F. Shannon ◽  
...  
Keyword(s):  
Human Cells ◽  
Interleukin 3 ◽  
And Function ◽  
Stimulation Of

Evolution and function of tandem repeats in the major surface protein 1a of the ehrlichial pathogenAnaplasma marginale

2001 ◽  
Vol 2 (2) ◽  
pp. 163-174 ◽  
Author(s):  
José de la Fuente ◽  
Jose C. Garcia-Garcia ◽  
Edmour F. Blouin ◽  
Sergio D. Rodríguez ◽  
Migel A. García ◽  
...  
Keyword(s):  
Tandem Repeats ◽  
Control Strategies ◽  
Surface Protein ◽  
Single Copy ◽  
Major Surface Protein ◽  
Host Parasite Interactions ◽  
Major Surface ◽  
And Function ◽  
Host Parasite ◽  
Bovine Erythrocytes

AbstractThe major surface protein (MSP) 1a of the ehrlichial cattle pathogenAnaplasma marginale, encoded by the single-copy genemsp1α, has been shown to have a neutralization-sensitive epitope and to be an adhesin for bovine erythrocytes and tick cells.msp1αhas been found to be a stable genetic marker for the identification of geographic isolates ofA. marginalethroughout development in acutely and persistently infected cattle and in ticks. The molecular weight of MSP1a varies among geographic isolates ofA. marginalebecause of a varying number of tandemly repeated peptides of 28–29 amino acids. Variation in the sequence of the tandem repeats occurs within and among isolates, and may have resulted from evolutionary pressures exerted by ligand–receptor and host–parasite interactions. These repeated sequences include markers for tick transmissibility that may be important in the identification of ehrlichial pathogens because they may influence control strategies and the design of subunit vaccines.

Abstract 15552: Acute Estrogen-GPER1 Stimulation Preserves Mitochondrial Inner Membrane Protein (Mitofilin) From Degradation caused by Ischemia/Reperfusion Stress

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Tanoya L. C Harris ◽  
Bjorn Olde ◽  
Fredrik Leeb-Lundberg ◽  
Jean C. Bopassa
Keyword(s):  
Electron Microscopy ◽  
Spatial Organization ◽  
Ischemia Reperfusion ◽  
Estrogen Treatment ◽  
Mitochondrial Inner Membrane ◽  
Mitochondrial Integrity ◽  
Inner Membrane Protein ◽  
Estrogen Effect ◽  
And Function ◽  
High Resolution Microscopy

Introduction: We recently found that acute estrogen treatment delays the mitochondrial permeability transition pore opening and reduces ROS production after ischemia/reperfusion, suggesting that estrogen promotes mitochondrial integrity. As mitochondrial inner membrane protein (mitofilin) has been found to control mitochondrial cristae morphology and function, we investigated whether estrogen effect on mitochondrial integrity after ischemia/reperfusion involved regulation of mitofilin via G-Protein Coupled Estrogen Receptor1 (GPER1) activation. Methods: Isolated hearts from male WT (C57BL/6NCrL), and GPER1-/- mice were perfused using Langendorff technique, with and without estrogen (40 nM). Hearts were subjected to 20 min global ischemia followed by 10 min reperfusion. Mitochondria were isolated, and 2D-DIGE followed by mass spectrometry was performed. Mitofilin expression was confirmed by Western blot analysis in mitochondrial fractions. Mitofilin distribution in cardiomyocytes, and its spatial organization in single mitochondria were visualized using high resolution microscopy. Electron microscopy was used to observe the state of mitochondrial cristae morphology. Results: Analysis revealded 52 unique proteins of interest, in which mitofilin was identified. Immunoblot analysis confirmed an increased in mitofilin level with estrogen treatment as compared to control in WT but not in GPER1-/-. We found, as observed in non-ischemic myocytes, that mitofilin in estrogen-treated cardiomyocytes was distributed in the peri-membrane and T-tubules, while only peri-membrane mitofilin was more visible in control group. High resolution microscopy showed a better spatial organization of mitofilin in single mitochondria with estrogen treatment compared to control, in which mitofilin was almost absent. Electron microscopy revealded that mitochondrial morphology was preserved with estrogen treatment, as cristae were well organized compared to control, in which cristae were disrupted. Conclusion: These data indicate that estrogen up-regulates mitofilin expression during ischemia/reperfusion. Estrogen effect on mitofilin may contribute to improved mitochondrial integrity and function.

Persistent expression of HNF6 in islet endocrine cells causes disrupted islet architecture and loss of beta cell function

Development ◽  
2000 ◽  
Vol 127 (13) ◽  
pp. 2883-2895 ◽  
Author(s):  
M. Gannon ◽  
M.K. Ray ◽  
K. Van Zee ◽  
F. Rausa ◽  
R.H. Costa ◽  
...  
Keyword(s):  
Beta Cell ◽  
Beta Cells ◽  
Endocrine Cells ◽  
Spatial Organization ◽  
Glucose Transporter ◽  
Cell Function ◽  
Regulatory Element ◽  
Cell Physiology ◽  
Pancreatic Ducts ◽  
And Function

We used transgenesis to explore the requirement for downregulation of hepatocyte nuclear factor 6 (HNF6) expression in the assembly, differentiation, and function of pancreatic islets. In vivo, HNF6 expression becomes downregulated in pancreatic endocrine cells at 18. 5 days post coitum (d.p.c.), when definitive islets first begin to organize. We used an islet-specific regulatory element (pdx1(PB)) from pancreatic/duodenal homeobox (pdx1) gene to maintain HNF6 expression in endocrine cells beyond 18.5 d.p.c. Transgenic animals were diabetic. HNF6-overexpressing islets were hyperplastic and remained very close to the pancreatic ducts. Strikingly, alpha, delta, and PP cells were increased in number and abnormally intermingled with islet beta cells. Although several mature beta cell markers were expressed in beta cells of transgenic islets, the glucose transporter GLUT2 was absent or severely reduced. As glucose uptake/metabolism is essential for insulin secretion, decreased GLUT2 may contribute to the etiology of diabetes in pdx1(PB)-HNF6 transgenics. Concordantly, blood insulin was not raised by glucose challenge, suggesting profound beta cell dysfunction. Thus, we have shown that HNF6 downregulation during islet ontogeny is critical to normal pancreas formation and function: continued expression impairs the clustering of endocrine cells and their separation from the ductal epithelium, disrupts the spatial organization of endocrine cell types within the islet, and severely compromises beta cell physiology, leading to overt diabetes.

scholarly journals The Intricate Role of p53 in Adipocyte Differentiation and Function

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2621
Author(s):  
Yun Kyung Lee ◽  
Yu Seong Chung ◽  
Ji Hye Lee ◽  
Jin Mi Chun ◽  
Jun Hong Park
Keyword(s):  
Adipocyte Differentiation ◽  
Metabolic Diseases ◽  
Metabolic Stress ◽  
Health Concern ◽  
Metabolic Dysfunction ◽  
Direct Role ◽  
Proliferation And Apoptosis ◽  
Response To Stress ◽  
And Function

For more than three decades, numerous studies have demonstrated the function of p53 in cell cycle, cellular senescence, autophagy, apoptosis, and metabolism. Among diverse functions, the essential role of p53 is to maintain cellular homeostatic response to stress by regulating proliferation and apoptosis. Recently, adipocytes have been studied with increasing intensity owing to the increased prevalence of metabolic diseases posing a serious public health concern and because metabolic dysfunction can directly induce tumorigenesis. The prevalence of metabolic diseases has steadily increased worldwide, and a growing interest in these diseases has led to the focus on the role of p53 in metabolism and adipocyte differentiation with or without metabolic stress. However, our collective understanding of the direct role of p53 in adipocyte differentiation and function remains insufficient. Therefore, this review focuses on the newly discovered roles of p53 in adipocyte differentiation and function.

scholarly journals YB-1 recruitment to stress granules in zebrafish cells reveals a differential adaptive response to stress

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Andrea Maria Guarino ◽  
Giuseppe Di Mauro ◽  
Gennaro Ruggiero ◽  
Nathalie Geyer ◽  
Antonella Delicato ◽  
...  
Keyword(s):  
Adaptive Response ◽  
Stress Granules ◽  
Response To Stress

scholarly journals Mitochondrial role in adaptive response to stress conditions in preeclampsia

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Polina A. Vishnyakova ◽  
Maria A. Volodina ◽  
Nadezhda V. Tarasova ◽  
Maria V. Marey ◽  
Daria V. Tsvirkun ◽  
...  
Keyword(s):  
Adaptive Response ◽  
Stress Conditions ◽  
Response To Stress

scholarly journals Photosynthetic hydrogen production by droplet-based microbial micro-reactors under aerobic conditions

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Zhijun Xu ◽  
Shengliang Wang ◽  
Chunyu Zhao ◽  
Shangsong Li ◽  
Xiaoman Liu ◽  
...  
Keyword(s):  
Hydrogen Production ◽  
Self Assembly ◽  
Spatial Organization ◽  
Oxygen Depletion ◽  
Bacterial Cells ◽  
Multicellular Spheroids ◽  
Two Phase ◽  
Aerobic Conditions ◽  
Micro Reactors ◽  
And Function

AbstractThe spontaneous self-assembly of multicellular ensembles into living materials with synergistic structure and function remains a considerable challenge in biotechnology and synthetic biology. Here, we exploit the aqueous two-phase separation of dextran-in-PEG emulsion micro-droplets for the capture, spatial organization and immobilization of algal cells or algal/bacterial cell communities to produce discrete multicellular spheroids capable of both aerobic (oxygen producing) and hypoxic (hydrogen producing) photosynthesis in daylight under air. We show that localized oxygen depletion results in hydrogen production from the core of the algal microscale reactor, and demonstrate that enhanced levels of hydrogen evolution can be achieved synergistically by spontaneously enclosing the photosynthetic cells within a shell of bacterial cells undergoing aerobic respiration. Our results highlight a promising droplet-based environmentally benign approach to dispersible photosynthetic microbial micro-reactors comprising segregated cellular micro-niches with dual functionality, and provide a step towards photobiological hydrogen production under aerobic conditions.

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