EAE of Mice: Enzymatic Cross Site-Specific Hydrolysis of H2A Histone by IgGs against H2A, H1, H2B, H3, and H4 Histones and Myelin Basic Protein Научная публикация
Журнал |
International Journal of Molecular Sciences
, E-ISSN: 1422-0067 |
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Вых. Данные | Год: 2023, Том: 24, Номер: 10, Номер статьи : 8636, Страниц : DOI: 10.3390/ijms24108636 | ||||
Ключевые слова | C57BL/6 mice; EAE model of human multiple sclerosis; immunization mice with MOG and DNA–histone complex; catalytic antibodies; hydrolysis of histones and myelin basic protein; cross-complexation and catalytic cross-reactivity | ||||
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Информация о финансировании (1)
1 | Российский научный фонд | РНФ №22-15-00103 |
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Open AccessArticle
EAE of Mice: Enzymatic Cross Site-Specific Hydrolysis of H2A Histone by IgGs against H2A, H1, H2B, H3, and H4 Histones and Myelin Basic Protein
by Andrey E. Urusov 1,Kseniya S. Aulova 1ORCID,Pavel S. Dmitrenok 2ORCID,Valentina N. Buneva 1ORCID andGeorgy A. Nevinsky 1,*ORCID
1
Institute of Chemical Biology and Fundamental Medicine of the Siberian Division of Russian Academy of Sciences, Novosibirsk 630090, Russia
2
G. B. Elyakov Pacific Institute of Bioorganic Chemistry, Far East Division, Russian Academy of Sciences, Vladivostok 690022, Russia
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2023, 24(10), 8636; https://doi.org/10.3390/ijms24108636
Submission received: 26 February 2023 / Revised: 6 April 2023 / Accepted: 10 April 2023 / Published: 12 May 2023
(This article belongs to the Collection Feature Paper Collection in Biochemistry)
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Abstract
Histones play vital roles in chromatin function and gene transcription; however, they are very harmful in the intercellular space because they stimulate systemic inflammatory and toxic responses. Myelin basic protein (MBP) is the major protein of the axon myelin–proteolipid sheath. Antibodies–abzymes with various catalytic activities are specific features of some autoimmune diseases. IgGs against individual histones (H2A, H1, H2B, H3, and H4) and MBP were isolated from the blood of experimental-autoimmune-encephalomyelitis-prone C57BL/6 mice by several affinity chromatographies. These Abs–abzymes corresponded to various stages of EAE development: spontaneous EAE, MOG, and DNA–histones accelerated the onset, acute, and remission stages. IgGs-abzymes against MBP and five individual histones showed unusual polyreactivity in the complex formation and enzymatic cross-reactivity in the specific hydrolysis of the H2A histone. All the IgGs of 3-month-old mice (zero time) against MBP and individual histones demonstrated from 4 to 35 different H2A hydrolysis sites. The spontaneous development of EAE over 60 days led to a significant change in the type and number of H2A histone hydrolysis sites by IgGs against five histones and MBP. Mice treatment with MOG and the DNA–histone complex changed the type and number of H2A hydrolysis sites compared to zero time. The minimum number (4) of different H2A hydrolysis sites was found for IgGs against H2A (zero time), while the maximum (35) for anti-H2B IgGs (60 days after mice treatment with DNA–histone complex). Overall, it was first demonstrated that at different stages of EAE evolution, IgGs–abzymes against individual histones and MBP could significantly differ in the number and type of specific sites of H2A hydrolysis. The possible reasons for the catalytic cross-reactivity and great differences in the number and type of histone H2A cleavage sites were analyzed.
Библиографическая ссылка:
Urusov A.E.
, Aulova K.S.
, Dmitrenok P.S.
, Buneva V.N.
, Nevinsky G.A.
EAE of Mice: Enzymatic Cross Site-Specific Hydrolysis of H2A Histone by IgGs against H2A, H1, H2B, H3, and H4 Histones and Myelin Basic Protein
International Journal of Molecular Sciences. 2023. V.24. N10. 8636 . DOI: 10.3390/ijms24108636 WOS
EAE of Mice: Enzymatic Cross Site-Specific Hydrolysis of H2A Histone by IgGs against H2A, H1, H2B, H3, and H4 Histones and Myelin Basic Protein
International Journal of Molecular Sciences. 2023. V.24. N10. 8636 . DOI: 10.3390/ijms24108636 WOS
Даты:
Опубликована в печати: | 12 мая 2024 г. |
Идентификаторы БД:
Web of science | WOS:000996874900001 |
OpenAlex | W4376278934 |
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Пока нет цитирований