Formyl peptide receptor-2 is upregulated in the blood and placenta of patients with gestational diabetes mellitus
- PMID: 34235813
- PMCID: PMC8519092
- DOI: 10.1111/jog.14927
Formyl peptide receptor-2 is upregulated in the blood and placenta of patients with gestational diabetes mellitus
Abstract
Aim: To investigate the expression of formyl peptide receptor 2 (FPR2) in maternal blood, umbilical blood, and placenta of patients with gestational diabetes mellitus (GDM), and to analyze the changes of other pro-inflammatory cytokines in blood, including interleukin 33 (IL-33), IL-1β, tumor necrosis factor alpha (TNF-α), and C-reactive protein (CRP), so as to reveal the pathogenesis of GDM.
Methods: FPR2, IL-33, IL-1β, T TNF-α, and CRP in maternal blood and umbilical cord blood of 50 pregnant women with GDM and 30 normal pregnant women were analyzed by ELISA method to explore the correlation between inflammatory factors and blood glucose. The expression of FPR2 in placental tissues was analyzed by PCR and immunohistochemistry.
Results: The expression of FPR2 in maternal blood of gestational diabetes patients was significantly higher than that of normal pregnant women, and other inflammatory factors IL-33 and IL-1β in maternal blood were also significantly increased. The expression of FPR2 in umbilical cord blood of gestational diabetes was higher than that of normal pregnant women, but the difference was not significant. Other inflammatory factors IL-33, IL-1β, and CRP in umbilical cord blood were also significantly increased. The expression of FPR2mRNA and protein in placental tissues of gestational diabetes was significantly higher than that of normal pregnant women.
Conclusions: The level of FPR2, IL-33, and IL-1β in maternal blood was related to the pathogenesis of GDM and these inflammatory factors could be used as special candidate direction of marks for the prevention, clinical treatment and drug design of GDM, laying a new theoretical foundation for the treatment of GDM.
Keywords: FPR2; GDM; inflammatory cytokines; pathogenesis.
© 2021 The Authors. Journal of Obstetrics and Gynaecology Research published by John Wiley & Sons Australia, Ltd on behalf of Japan Society of Obstetrics and Gynecology.
Conflict of interest statement
All authors declare no conflict of interest for this work.
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