Expression level of genes encoding components of the purinergic pathway and cryopyrin in essential arterial hypertension
https://doi.org/10.25557/2073-7998.2025.09.128-130
Abstract
Background. Increased extracellular ATP is associated with activation of the NLRP3 inflammasome, production of proinflammatory cytokines and development of inflammation. Ectonucleotidases CD39 and CD73, adenosine receptors located on the surface of some immune cells, participate in the regulation of extracellular ATP levels and the adenosinergic signaling pathway. However, information on the expression level of genes encoding these enzymes (ENTPD1 (CD39), NT5E (CD73)) and adenosine receptors in essential arterial hypertension (EAH) is still scarce.
Objective. Determination of the mRNA level of genes encoding proteins of the purinergic signaling pathway (ENTPD1, NT5E, ADORA2A) and the NLRP3 gene in peripheral blood leukocytes (PBL) of patients with EAH.
Patients and methods. The study involved 16 healthy individuals, 17 patients with EAH (stages I-II) (including 8 people before the prescription of antihypertensive drugs and 9 people taking metoprolol (25 mg/day) or bisoprolol (5-10 mg/day) for more than a year). The relative level of gene transcripts was determined by real-time PCR.
Results. The level of the ENTPD1, NT5E, ADORA2A, NLRP3 gene expression in PBL of patients with EAH was higher than in healthy people (p<0,01). The level of NLRP3 gene expression was closely associated with the relative mRNA content of the ENTPD1, NT5E, ADORA2A genes (respectively, r=0,77; 0,66; 0,72; p<0,01).
Conclusion. The formation of EAH is accompanied by an increase in the ENTPD1, NT5E, ADORA2A, NLRP3 genes expression level, which probably reflects the activation of the purinergic signaling pathway in this disease.
About the Authors
L. V. TopchievaRussian Federation
11,Pushkinskaya st., Petrozavodsk, 185910
V. A. Korneva
Russian Federation
33, Lenina st., Petrozavodsk, 185910
D. A. Atorin
Russian Federation
11,Pushkinskaya st., Petrozavodsk, 185910
G. A. Zhulai
Russian Federation
11,Pushkinskaya st., Petrozavodsk, 185910
I. V. Kurbatova
Russian Federation
11,Pushkinskaya st., Petrozavodsk, 185910
References
1. Burnstock G., Pelleg A. Cardiac purinergic signalling in health and disease. Purinergic Signalling. 2015;11:1-46. doi: 10.1007/s11302-014-9436-1
2. Ratajczak M.Z., Kucia M. Extracellular adenosine triphosphate (eATP) and its metabolite, extracellular adenosine (eado), as opposing «yin–yang» regulators of Nlrp3 inflammasome in the trafficking of hematopoietic stem/progenitor cells. Front. Immunol. 2021;11:603942. doi: 10.3389/fimmu.2020.603942
3. Topchieva L.V., Kurbatova I.V., Malysheva I.E. et al. Allel’nyy polimorfizm genov, vovlechennykh v produktsiyu IL-1b, i predraspolozhennost’ lyudey k razvitiyu arterial’noy gipertenzii [Allelic polymorphism of genes involved in IL-1β production and predisposition of people to the development of arterial hypertension]. Nauchnyye rezul’taty biomeditsinskikh issledovaniy [Scientific results of biomedical research]. 2023;9(1):53-70. (In Russ.) doi: 10.18413/2658-6533-2023-9-1-0-4
4. Atorin D.A., Zhulai G.A., Tophieva L.V., et al. Uroven’ ekspressii genov ENTPD1, NT5E, ADORA2A, FOXP3 i RORg v perifericheskoy krovi bol’nykh yazvennym kolitom [ENTPD1, NT5E, ADORA2A, FOXP3 and RORγ gene expression in peripheral blood of patients with ulcerative colitis]. Meditsinskaya immunologiya [Medical Immunology (Russia)]. 2025;27(1):197-206. (In Russ.) https://doi.org/10.15789/1563-0625-ENA-2976
5. Higashikuni Y., Liu W., Numata G., et al. NLRP3 inflammasome activation through heart-brain interaction initiates cardiac inflammation and hypertrophy during pressure overload. Circulation. 2023;147(4):338- 355. doi: 10.1161/CIRCULATIONAHA.122.060860
Review
For citations:
Topchieva L.V., Korneva V.A., Atorin D.A., Zhulai G.A., Kurbatova I.V. Expression level of genes encoding components of the purinergic pathway and cryopyrin in essential arterial hypertension. Medical Genetics. 2025;24(9):128-130. (In Russ.) https://doi.org/10.25557/2073-7998.2025.09.128-130






















