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23 results on '"Veremeyko, Tatyana"'

7. Sex-Specific ADHD-like Behaviour, Altered Metabolic Functions, and Altered EEG Activity in Sialyltransferase ST3GAL5-Deficient Mice

Author

Strekalova, Tatyana, primary, Veniaminova, Ekaterina, additional, Svirin, Evgeniy, additional, Kopeikina, Ekaterina, additional, Veremeyko, Tatyana, additional, Yung, Amanda W. Y., additional, Proshin, Andrey, additional, Tan, Shawn Zheng Kai, additional, Khairuddin, Sharafuddin, additional, Lim, Lee Wei, additional, Lesch, Klaus-Peter, additional, Walitza, Susanne, additional, Anthony, Daniel C., additional, and Ponomarev, Eugene D., additional

Published
2021
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8. Sex-Specific ADHD-like Behaviour, Altered Metabolic Functions, and Altered EEG Activity in Sialyltransferase ST3GAL5-Deficient Mice

Author

Strekalova, Tatyana, Veniaminova, Ekaterina, Svirin, Evgeniy; https://orcid.org/0000-0003-3501-574X, Kopeikina, Ekaterina, Veremeyko, Tatyana, Yung, Amanda W Y, Proshin, Andrey; https://orcid.org/0000-0002-7258-7870, Tan, Shawn Zheng Kai; https://orcid.org/0000-0001-7258-9596, Khairuddin, Sharafuddin, Lim, Lee Wei; https://orcid.org/0000-0001-6692-6285, Lesch, Klaus-Peter, Walitza, Susanne, Anthony, Daniel C; https://orcid.org/0000-0003-1380-6655, Ponomarev, Eugene D, Strekalova, Tatyana, Veniaminova, Ekaterina, Svirin, Evgeniy; https://orcid.org/0000-0003-3501-574X, Kopeikina, Ekaterina, Veremeyko, Tatyana, Yung, Amanda W Y, Proshin, Andrey; https://orcid.org/0000-0002-7258-7870, Tan, Shawn Zheng Kai; https://orcid.org/0000-0001-7258-9596, Khairuddin, Sharafuddin, Lim, Lee Wei; https://orcid.org/0000-0001-6692-6285, Lesch, Klaus-Peter, Walitza, Susanne, Anthony, Daniel C; https://orcid.org/0000-0003-1380-6655, and Ponomarev, Eugene D

Abstract

A deficiency in GM3-derived gangliosides, resulting from a lack of lactosylceramide-alpha-2,3-sialyltransferase (ST3GAL5), leads to severe neuropathology, including epilepsy and metabolic abnormalities. Disruption of ganglioside production by this enzyme may also have a role in the development of neuropsychiatric disorders. ST3Gal5 knock-out (St3gal5−/−) mice lack a-, b-, and c-series gangliosides, but exhibit no overt neuropathology, possibly owing to the production of compensatory 0-series glycosphingolipids. Here, we sought to investigate the possibility that St3gal5−/− mice might exhibit attention-deficit/hyperactivity disorder (ADHD)-like behaviours. In addition, we evaluated potential metabolic and electroencephalogram (EEG) abnormalities. St3gal5−/− mice were subjected to behavioural testing, glucose tolerance tests, and the levels of expression of brain and peripheral A and B isoforms of the insulin receptor (IR) were measured. We found that St3gal5−/− mice exhibit locomotor hyperactivity, impulsivity, neophobia, and anxiety-like behavior. The genotype also altered blood glucose levels and glucose tolerance. A sex bias was consistently found in relation to body mass and peripheral IR expression. Analysis of the EEG revealed an increase in amplitude in St3gal5−/− mice. Together, St3gal5−/− mice exhibit ADHD-like behaviours, altered metabolic and EEG measures providing a useful platform for better understanding of the contribution of brain gangliosides to ADHD and associated comorbidities. Keywords: lactosylceramide alpha-2,3-sialyltransferase (ST3GAL5); attention-deficit/hyperactivity disorder (ADHD); insulin receptor (IR); sex differences; electroencephalogram (EEG); mice

Published
2021

9. MicroRNA-124 promotes microglia quiescence and suppresses EAE by deactivating macrophages via the C/EBP-α-PU.1 pathway

Author

Ponomarev, Eugene D., Veremeyko, Tatyana, Barteneva, Natasha, Krichevsky, Anna M., and Weiner, Howard L.

Subjects
Inflammation -- Control, Cell cycle -- Research, MicroRNA -- Health aspects, Macrophages -- Health aspects, Biological sciences, Health
Abstract

MicroRNAs are a family of regulatory molecules involved in many physiological processes, including differentiation and activation of cells of the immune system. We found that brain-specific miR-124 is expressed in microglia but not in peripheral monocytes or macrophages. When overexpressed in macrophages, miR-124 directly inhibited the transcription factor CCAAT/enhancerbinding protein-α (C/EBP-α) and its downstream target PU.1, resulting in transformation of these cells from an activated phenotype into a quiescent [CD45.sup.low,] major histocompatibility complex (MHC) class [II.sup.low] phenotype resembling resting microglia. During experimental autoimmune encephalomyelitis (EAE), miR-124 was downregulated in activated microglia. Peripheral administration of miR-124 in EAE caused systemic deactivation of macrophages, reduced activation of myelin-specific T cells and marked suppression of disease. Conversely, knockdown of miR-124 in microglia and macrophages resulted in activation of these cells in vitro and in vivo. These findings identify miR-124 both as a key regulator of microglia quiescence in the central nervous system and as a previously unknown modulator of monocyte and macrophage activation., MicroRNAs (miRNAs) belong to a family of small non-protein-coding RNAs that regulate expression of multiple target genes and are involved in many fundamental biological processes, such as embryonic development, cell [...]

Published
2011
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14. Cyclic AMP Pathway Suppress Autoimmune Neuroinflammation by Inhibiting Functions of Encephalitogenic CD4 T Cells and Enhancing M2 Macrophage Polarization at the Site of Inflammation

Author

Veremeyko, Tatyana, primary, Yung, Amanda W. Y., additional, Dukhinova, Marina, additional, Kuznetsova, Inna S., additional, Pomytkin, Igor, additional, Lyundup, Alexey, additional, Strekalova, Tatyana, additional, Barteneva, Natasha S., additional, and Ponomarev, Eugene D., additional

Published
2018
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23. The Emerging Role of Immunoglobulins and Complement in the Stimulation of Neuronal Activity and Repair: Not as Simple as We Thought.

Author

Veremeyko T, Barteneva NS, Vorobyev I, and Ponomarev ED

Subjects
Humans, Animals, Immunoglobulins metabolism, Immunoglobulins immunology, Neurodegenerative Diseases metabolism, Neurodegenerative Diseases immunology, Neurons metabolism, Complement System Proteins immunology, Complement System Proteins metabolism
Abstract

Neurologic disorders such as traumatic brain injury, multiple sclerosis, Alzheimer's disease, and drug-resistant epilepsy have a high socioeconomic impact around the world. Current therapies for these disorders are often not effective. This creates a demand for the development of new therapeutic approaches to treat these disorders. Recent data suggest that autoreactive naturally occurring immunoglobulins produced by subsets of B cells, called B1 B cells, combined with complement, are actively involved in the processes of restoration of neuronal functions during pathological conditions and remyelination. The focus of this review is to discuss the possibility of creating specific therapeutic antibodies that can activate and fix complement to enhance neuronal survival and promote central nervous system repair after injuries associated with many types of neurodegenerative diseases.

Published
2024
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