Tatsiana G. Dubouskaya

Institute of Biophysics and Cell Engineering

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Sergei V. Fedorovich

Institute of Biophysics and Cell Engineering

Sviatlana V. Hrynevich

Belarusian State University

Tatyana V. Waseem

University of Oxford

L.A. Volianska

I.Horbachevsky Ternopil National Medical University

Mikhail Belevtsev

Belarusian Research Center For Pediatric Oncology and Hematology

Jessica Mitlöhner

Leibniz Institute for Neurobiology

Rafaella A. Gonçalves

Queen's University

Behnam Vafadari

University of Göttingen

Mikhail V. Goltsev

Belarusian State Medical University

Svetlana O. Sharapova

Belarusian Research Center For Pediatric Oncology and Hematology

Cooperative Institutions

Belarusian Research Center For Pediatric Oncology and Hematology

Institute of Biophysics and Cell Engineering

National Academy of Sciences of Belarus

Shupyk National Healthcare University of Ukraine

Belarusian State Medical University

Institute of Pediatrics, Obstetrics, and Gynecology named after acad. O.M. Lukyanova of the National Academy of Medical Sciences of Ukraine

Belarusian State University

Universidade Federal do Rio de Janeiro

Columbia University Irving Medical Center

European University

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Variable CD18 expression in a 22‐year‐old female with leukocyte adhesion deficiency I: Clinical case and literature review

Clinical Case Reports (2023)

Анастасія Бондаренко Oksana Boyarchuk Inga Sakovich Ekaterina Polyakova Alexander A. Migas

Partial leukocyte adhesion deficiency type 1 (LAD-1) deficiency is extremely rare condition with milder infectious manifestation and immune system imbalance leads to increased risks of autoinflammatory complications, such as pyoderma gangrenosum, that can be triggered by trauma or pregnancy. In patients with spice-site ITGB2 variants, partial expression can occur due to different β2 integrin isophorms expression.

Leukocyte adhesion deficiency

Expression (computer science)

10.1002/ccr3.7791

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Calcium release from intracellular stores is involved in mitochondria depolarization after lowering extracellular pH in rat brain synaptosomes

Acta Neurobiologiae Experimentalis (2018)

Tatsiana G. Dubouskaya Sviatlana V. Hrynevich Tatyana V. Waseem Sergei V. Fedorovich

In the brain, pH can be lowered in both healthy and disease states. Previously, we showed that moderate extracellular acidification (down to pHo 7.0), but not intracellular acidification, leads to mitochondrial depolarization in synaptosomes. This indicates that the plasma membranes of neuronal presynaptic endings have proton receptors that can induce mitochondrial dysfunction when activated. In the present paper we attempt to identify this hypothetical receptor. First, we have demonstrated that lowering pHo to 7.0 does not induce sodium influx as monitored by the fluorescent dye Sodium Green. This fact, in conjunction with the absence of calcium influx in the same conditions - demonstrated previously, excludes ion channels as possible receptors. However, we showed that acidification-induced mitochondrial depolarization is sensitive to thapsigargin - an inhibitor of calcium release from intracellular stores, U73122 - an inhibitor of phospholipase C, as well as Cu2+ and Zn2+, which can block the metabotropic proton receptor ovarian cancer G protein-coupled receptor 1 (OGR1). Furthermore, using fluorescent dye Fluo-3 we have demonstrated that moderate extracellular acidification induces a cytosolic calcium increase. Excess calcium was scavenged by mitochondria (monitored by fluorescent dye Rhod-2). Our results suggest that the metabotropic OGR1 is a hypothetical presynaptic receptor for low pH. Its activation leads to phospholipase C activation and calcium release from the endoplasmic reticulum followed by accumulation in mitochondria, which likely causes a decrease in mitochondrial membrane potential.

Thapsigargin

10.21307/ane-2018-033

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High Concentration of Ketone Body β-Hydroxybutyrate Modifies Synaptic Vesicle Cycle and Depolarizes Plasma Membrane of Rat Brain Synaptosomes

Journal of Molecular Neuroscience (2019)

Polina P. Voronina Ksenia V. Adamovich Tatyana V. Adamovich Tatsiana G. Dubouskaya Sviatlana V. Hrynevich

Synaptosome

Acridine orange

10.1007/s12031-019-01406-9

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The energetic brain – A review from students to students

Journal of Neurochemistry (2019)

Melina Bordone Mootaz M. Salman Haley E. Titus Elham Amini Jens V. Andersen

Abstract The past 20 years have resulted in unprecedented progress in understanding brain energy metabolism and its role in health and disease. In this review, which was initiated at the 14th International Society for Neurochemistry Advanced School, we address the basic concepts of brain energy metabolism and approach the question of why the brain has high energy expenditure. Our review illustrates that the vertebrate brain has a high need for energy because of the high number of neurons and the need to maintain a delicate interplay between energy metabolism, neurotransmission, and plasticity. Disturbances to the energetic balance, to mitochondria quality control or to glia–neuron metabolic interaction may lead to brain circuit malfunction or even severe disorders of the CNS . We cover neuronal energy consumption in neural transmission and basic (‘housekeeping’) cellular processes. Additionally, we describe the most common (glucose) and alternative sources of energy namely glutamate, lactate, ketone bodies, and medium chain fatty acids. We discuss the multifaceted role of non‐neuronal cells in the transport of energy substrates from circulation (pericytes and astrocytes) and in the supply (astrocytes and microglia) and usage of different energy fuels. Finally, we address pathological consequences of disrupted energy homeostasis in the CNS . image

Energy homeostasis

10.1111/jnc.14829

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Citations (165)