IMR Press / FBL / Volume 28 / Issue 1 / DOI: 10.31083/j.fbl2801007
Open Access Original Research
β-arrestin2 Mediates the Arginine Vasopressin-Induced Expression of IL-1β in Murine Hearts
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1 Cardiovascular Laboratory, Department of Pharmacology, School of Pharmacy, Nantong University, 226001 Nantong, Jiangsu, China
2 Affiliated Hospital of Nantong University, 226001 Nantong, Jiangsu, China
*Correspondence: (Weizhong Zhu)
These authors contributed equally.
Academic Editors: Md Soriful Islam and Most Mauluda Akhtar
Front. Biosci. (Landmark Ed) 2023, 28(1), 7;
Submitted: 16 July 2022 | Revised: 11 November 2022 | Accepted: 11 November 2022 | Published: 10 January 2023
Copyright: © 2023 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.

Background: Circulating levels of arginine vasopressin (AVP) are elevated during cardiac stress and this could be a factor in cardiac inflammation and fibrosis. Herein, we studied the effects of AVP on interleukin-1β (IL-1β) production and the role(s) of β-arrestin2-dependent signaling in murine heart. Methods: The levels of IL-1β mRNA and protein in adult rat cardiofibroblasts (ARCFs) was measured using quantitative PCR and ELISA, respectively. The activity of β-arrestin2 was manipulated using either pharmacologic inhibitors or through recombinant β-arrestin2 over-expression. These experiments were conducted to determine the roles of β-arrestin2 in the regulation of AVP-induced IL-1β and NLRP3 inflammasome production. The phosphorylation and activation of NF-κB induced by AVP was measured by immunoblotting. β-arrestin2 knockout (KO) mice were used to investigate whether β-arrestin2 mediated the AVP-induced production of IL-1β and NLRP3, as well as the phosphorylation of the NF-κB p65 subunitin mouse myocardium. Prism GraphPad software(version 8.0), was used for all statistical analyses. Results: AVP induced the expression of IL-1β in a time-dependent manner in ARCFs but not in cultured adult rat cardiomyocytes (ARCMs). The inhibition of NF-κB with pyrrolidinedithiocarbamic acid (PDTC) prevented the AVP-induced phosphorylation of NF-κB and production of IL-1β and NLRP3 in ARCFs. The deletion of β-arrestin2 blocked the phosphorylation of p65 and the expression of NLRP3 and IL-1β induced by AVP in both mouse hearts and in ARCFs. Conclusions: AVP promotes IL-1β expression through β-arrestin2-mediated NF-κB signaling in murine heart.

arginine vasopressin
β-arrestin 2
NF-κB p65
NLRP3 inflammasome
81770400/National Natural Science Foundation of China
JCZ18131/Nantong Municipal Science and Technology
JC2019133/Nantong Municipal Science and Technology
Fig. 1.
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