vavilovВавиловский журнал генетики и селекцииVavilov Journal of Genetics and Breeding2500-3259Institute of Cytology and Genetics of Siberian Branch of the RAS10.18699/vjgb-25-16vavilov-4485Research ArticleБИОТЕХНОЛОГИЯ В ПОСТГЕНОМНУЮ ЭРУMEDICAL GENETICSРоль полиморфизма гена SELE при инфаркте миокарда с подъемом сегмента STThe role of SELE gene polymorphism in ST-elevation myocardial infarctionhttps://orcid.org/0000-0001-6133-8986БабушкинаН. П.BabushkinaN. P.

Томск

Tomsk

nad.babushkina@medgenetics.ruhttps://orcid.org/0000-0002-1632-6342НиколаеваА. М.NikolaevaA. M.

Томск

Tomsk

ДолбняА. Д.DolbnyaA. D.

Томск

Tomsk

ШавракВ. Е.ShavrakV. E.

Томск

Tomsk

РябовВ. В.RyabovV. V.

Томск

Tomsk

Научно-исследовательский институт медицинской генетики, Томский национальный исследовательский медицинский центр Российской академии наукРоссияResearch Institute of Medical Genetics, Tomsk National Research Medical Center of the Russian Academy of SciencesRussian FederationНаучно-исследовательский институт кардиологии, Томский национальный исследовательский медицинский центр Российской академии наукРоссияCardiology Research Institute, Tomsk National Research Medical Center of the Russian Academy of SciencesRussian FederationСибирский государственный медицинский университет Министерства здравоохранения Российской ФедерацииРоссияSiberian State Medical University of the Ministry of Healthcare of the Russian FederationRussian FederationНациональный исследовательский Томский государственный университетРоссияTomsk State UniversityRussian FederationНаучно-исследовательский институт кардиологии, Томский национальный исследовательский медицинский центр Российской академии наук; Сибирский государственный медицинский университет Министерства здравоохранения Российской Федерации; Национальный исследовательский Томский государственный университетРоссияCardiology Research Institute, Tomsk National Research Medical Center of the Russian Academy of Sciences; Siberian State Medical University of the Ministry of Healthcare of the Russian Federation; Tomsk State UniversityRussian Federation202504032025291135143Copyright © Бабушкина Н.П., Николаева А.М., Долбня А.Д., Шаврак В.Е., Рябов В.В., 20252025Бабушкина Н.П., Николаева А.М., Долбня А.Д., Шаврак В.Е., Рябов В.В.Babushkina N.P., Nikolaeva A.M., Dolbnya A.D., Shavrak V.E., Ryabov V.V.This work is licensed under a Creative Commons Attribution 4.0 License.https://vavilov.elpub.ru/jour/article/view/4485

   Ишемическая болезнь сердца представляет собой важную медико-социальную проблему. Наиболее тяжелой формой заболевания, с поражением всех слоев сердечной мышцы, считается инфаркт миокарда с подъемом сегмента ST (ИМпST). Одним из диагностических критериев дисфункции эндотелия при инфаркте миокарда является уровень sE-селектина – молекулы клеточной адгезии, осуществляющей рекрутинг нейтрофилов и индукцию нейтрофильного воспаления. В настоящем исследовании изучен интронный полиморфизм (rs5353, rs3917412, rs1534904) гена SELE, кодирующего Е-селектин, у пациентов с ИМпST. Проанализированы две выборки: пациенты с ИМпST (n = 74) и популяционная выборка г. Томска (n = 136). По частотам генотипов rs5353 в гене SELE зарегистрированы статистически значимые различия между пациентами и контрольной выборкой (p = 0.004). Генотип СС является рисковым по отношению к ИМпST (OR = 6.93, CI:95 % (1.84–26.04), χ2 = 8.69, p = 0.002). Проанализированные маркеры не изучались ранее при сердечно-сосудистых заболеваниях и вообще редко привлекались к ассоциативным исследованиям; в ведущих базах данных отсутствует информация об ассоциациях этих маркеров с заболеваниями. Вместе с тем все три варианта по классификации RegulomeDB относятся к функциональному классу 1f и, соответственно, с высокой вероятностью обладают регуляторным потенциалом относительно не только гена SELE, но и других генов близлежащего региона. Анализ функциональной значимости изученных маркеров показал наличие более обширного, чем один ген, региона, корегулируемого данными нуклеотидными заменами. Выявленная в настоящем исследовании ассоциация rs5353 с ИМпST еще раз подтверждает вовлеченность гена SELE в развитие сердечно-сосудистых заболеваний. Не исключено, что опосредованно (через системы воспаления, иммунного ответа и репарации ДНК) весь этот регион генома может быть вовлечен в патогенез сердечно-сосудистых заболеваний.

   Ischemic heart disease (IHD) is an important medical and social problem. ST-elevation myocardial infarction (STEMI) is the most severe form of IHD, affecting all layers of the heart muscle. One of the diagnostic criteria for endothelial dysfunction in myocardial infarction is the level of sE-selectin, a cell adhesion molecule that recruits neutrophils and induces neutrophil inflammation.

   The aim of this study is to investigate intronic polymorphisms rs5353, rs3917412 and rs1534904 of the E-selectin coding gene SELE in patients with STEMI. We have analyzed a group of patients with STEMI (n = 74) and a population sample of Tomsk (n = 136) as the control group.

   The frequencies of the rs5353 genotypes in the SELE gene have shown statistically significant differences between patients and the control sample (p = 0.004). The CC genotype is a predisposing factor to STEMI (OR = 6.93, CI:95 % (1.84–26.04), χ2 = 8.69, p = 0.002). The analyzed mar kers were not studied previously in cardiovascular diseases (CVDs) and were rarely involved in association studies at all; there is no information on these SNPs in the leading databases. At the same time, all three variants, according to the RegulomeDB classification, belong to the functional class 1f, and are highly likely to have regulatory potential relative not only to the SELE gene, but also to other genes in the nearby region. The analysis of the functional significance of the studied markers has shown the presence of a region more extensive than one gene, which is co-regulated by the studied nucleotide substitutions. The association of rs5353 with STEMI identified in this study once again confirms the involvement of the SELE gene in the pathogenesis of CVDs. It is possible that this entire region of the genome may be involved indirectly in the pathogenesis of CVD through the systems of inflammation, immune response and DNA repair.

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The authors declare that there are no conflicts of interest present.