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Investigation of the effects of urotensin II receptors in LPS-induced inflammatory response in HUVEC cell line through calcineurin/NFATc/IL-2 pathway

Advances in Medical Sciences · Eylül 2023

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YÖKSİS Kayıtları
Investigation of the effects of urotensin II receptors in LPS-induced inflammatory response in HUVEC cell line through calcineurin/NFATc/IL-2 pathway
Advances in Medical Sciences · 2023 SCI-Expanded
DOKTOR ÖĞRETİM ÜYESİ MUHAMMED YAYLA →

Makale Bilgileri

DergiAdvances in Medical Sciences
Yayın TarihiEylül 2023
Cilt / Sayfa68 · 433-440
Özet Purpose: The effect of urotensin II (U-II), a powerful endogenous vasoconstrictor substance, on the immune system and its mediators is very important. It was herein aimed to demonstrate the possible relationship between the calcineurin/nuclear factor of activated T-cells cytoplasmic 1/interleukin-2 (CaN/NFATc/IL-2) pathway and urotensin receptors (UTRs) in inflammatory response due to lipopolysaccharide (LPS). Methods: An LPS-induced inflammation model was used on the human umbilical vein endothelial cells (HUVEC) cell line and drugs were applied accordingly, forming the following groups: Control Group, LPS Group, Agonist Group (10−8 ​M U-II), Antagonist Group (10−6 ​M palosuran), Tacrolimus (TAC) Group (10 ​ng/mL FK-506), Agonist ​+ ​TAC Group, and Antagonist ​+ ​TAC Group. Gene expression analyses were performed using real-time polymerase chain reaction (RT-PCR). Results: In the analysis of the cell viability at 48 and 72 ​h, there was a decrease in the Agonist Group, while in the Agonist ​+ ​TAC Group, the cell viability increased. In the Antagonist Group, cell viability was maintained when compared to the LPS Group, while in the TAC Group, this effect was reduced. The mRNA expression levels of UTR, CaN, NFATc, IL-2 receptor (IL-2R), IL-6 and nuclear factor kappa B (NF-κB) were higher in the LPS Group than in the Control Group, and even the UTR, CaN, NFATc, IL-2R were higher with agonist administration. This effect of the agonist was shown to be completely mitigated in the presence of the CaN inhibitor. Conclusion: U-II and its receptors can perform key functions regarding the endothelial cell damage via the CaN/NFATc/IL-2 pathway.

Yazarlar (4)

1
Zekai Halici
2
Vedat Bulut
3
Elif Cadirci
4
Muhammed Yayla
ORCID: 0000-0002-0659-3084

Anahtar Kelimeler

Calcineurin HUVEC Inflammation NFATc Urotensin II

Kurumlar

Atatürk Üniversitesi
Erzurum Turkey
Gazi Üniversitesi
Ankara Turkey
Kafkas Üniversitesi
Kars Turkey