AT-rich interactive domain-containing protein 1A (ARID1A) expression in placentas with late fetal growth restriction
- Authors: Tral T.G.1, Yusenko S.R.1, Tolibova G.K.1, Kogan I.Y.1
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Affiliations:
- The Research Institute of Obstetrics, Gynecology and Reproductology named after D.O. Ott
- Issue: Vol 73, No 2 (2024)
- Pages: 99-108
- Section: Original Research
- Submitted: 29.02.2024
- Accepted: 12.03.2024
- Published: 27.05.2024
- URL: https://journals.eco-vector.com/jowd/article/view/627609
- DOI: https://doi.org/10.17816/JOWD627609
- ID: 627609
Cite item
Abstract
BACKGROUND: Fetal growth restriction, which is considered as a multifactorial pathology, is a critical problem in obstetrics. The role of mitochondrial dysfunction in the pathogenesis of fetal growth restriction is not yet clear. However, it is known that it leads to oxidative stress, damage to cells and tissues, and dysfunction of key mechanisms for maintaining energy balance, the outcome of which may be the development of placental insufficiency. It is likely that AT-rich interactive domain-containing protein 1A (ARID1A) is involved in the development and function of the human placenta and may be an important marker in the development of fetal growth restriction.
AIM: The aim of this study was to evaluate ARID1A protein expression in the placental villous tree in late fetal growth restriction.
MATERIALS AND METHODS: This study included 50 placentas from children born at full-term gestation (37–40 weeks). The main study group consisted of placentas with late fetal growth restriction and without major extragenital pathology (n = 35). The control group comprised 15 placentas without fetal growth restriction (n = 15). Histological (n = 50) and immunohistochemical examinations of placentas (15 placentas in the main group and 10 placentas in the control group) using primary monoclonal antibodies to ARID1A were performed.
RESULTS: In the study group with fetal growth restriction, chronic placental insufficiency was verified in all cases, dissociated chronic placental insufficiency (25 cases; 71.4%) being predominant, of which 23 cases (92%) were compensated, including 16 cases (69.6%) with moderate circulatory disorders. Hypoplastic chronic placental insufficiency was diagnosed in ten cases (28.6%) and was subcompensated with the presence of pronounced circulatory disorders. In the arteries of the stem villi, the ARID1A protein expression area did not differ between the study groups (p = 0.096), while in the veins in the stem villi with fetal growth restriction, we verified a decrease compared to control (p = 0.05). In the vascular bed of the villi with subcompensated dissociated chronic placental insufficiency, ARID1A protein expression was higher compared to hypoplastic chronic placental insufficiency (p = 0.041).
CONCLUSIONS: Chronic placental insufficiency combined with fetal growth restriction is a serious complication of pregnancy with the development of structural and functional abnormalities and dysregulation of placental mechanisms. The ARIDA1A protein expression data obtained, depending on the degree of compensation for chronic placental insufficiency, may indicate the activation of compensatory metabolic mechanisms to maintain the functional activity of the placenta and preserve the viability of the fetus.
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About the authors
Tatiana G. Tral
The Research Institute of Obstetrics, Gynecology and Reproductology named after D.O. Ott
Author for correspondence.
Email: ttg.tral@yandex.ru
ORCID iD: 0000-0001-8948-4811
SPIN-code: 1244-9631
Scopus Author ID: 37666260400
MD, Cand. Sci. (Med.)
Russian Federation, 3 Mendeleevskaya Line, Saint Petersburg, 199034Sofia R. Yusenko
The Research Institute of Obstetrics, Gynecology and Reproductology named after D.O. Ott
Email: iusenko.sr@gmail.com
ORCID iD: 0000-0001-7316-8179
MD, postgraduate student
Russian Federation, 3 Mendeleevskaya Line, Saint Petersburg, 199034Gulrukhsor Kh. Tolibova
The Research Institute of Obstetrics, Gynecology and Reproductology named after D.O. Ott
Email: gulyatolibova@mail.ru
ORCID iD: 0000-0002-6216-6220
SPIN-code: 7544-4825
Scopus Author ID: 23111355700
ResearcherId: Y-6671-2018
MD, Dr. Sci. (Med)
Russian Federation, 3 Mendeleevskaya Line, Saint Petersburg, 199034Igor Yu. Kogan
The Research Institute of Obstetrics, Gynecology and Reproductology named after D.O. Ott
Email: ikogan@mail.ru
ORCID iD: 0000-0002-7351-6900
SPIN-code: 6572-6450
Scopus Author ID: 56895765600
ResearcherId: P-4357-2017
MD, Dr. Sci. (Med.), Professor, Corresponding Member of the Russian Academy of Sciences
Russian Federation, 3 Mendeleevskaya Line, Saint Petersburg, 199034References
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