The Role of the Aryl Hydrocarbon Receptor in Vascular Factors Related to Preeclampsia in a Smoking Mouse Modelopen access
- Authors
- Kim, Ho-Yeon; Seok, Ye-Seon; Moon, Hye-Yeon; Cho, Geum-Joon; Ahn, Ki-Hoon; Hong, Soon-Cheol; Oh, Min-Jeong; Kim, Hai-Joong
- Issue Date
- Jan-2024
- Publisher
- MDPI
- Keywords
- aryl hydrocarbon receptor; soluble FMS-like tyrosine kinase; cigarette
- Citation
- Current Issues in Molecular Biology, v.46, no.1, pp 741 - 752
- Pages
- 12
- Indexed
- SCIE
SCOPUS
- Journal Title
- Current Issues in Molecular Biology
- Volume
- 46
- Number
- 1
- Start Page
- 741
- End Page
- 752
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2021.sw.kumedicine/65421
- DOI
- 10.3390/cimb46010048
- ISSN
- 1467-3037
1467-3045
- Abstract
- Smoking cigarettes is known to lower the risk of preeclampsia. The objective of this study is to evaluate the effect of smoking on the expression of soluble FMS-like tyrosine kinase-1 (sFlt-1), vascular endothelial growth factor (VEGF), and endoglin (sEng)-1 and the role of the aryl hydrocarbon receptor (AhR) in pregnant mice. We developed a smoking mouse model using a gas-filling system. One or two cigarettes per day were exposed to each of the five pregnant mice for five days a week throughout pregnancy. AhR agonist and antagonist were injected. Serum levels and expression in the placenta of sFlt-1, VEGF, and sEng-1 were analyzed and compared among the cigarette smoke and no-exposure groups after delivery. Compared to the no-smoke exposure group, the serum level of sFlt-1 was significantly decreased in the two-cigarette-exposed group (p < 0.001). When the AhR antagonist was added to the two-cigarette-exposed group, sFlt-1 levels were significantly increased compared to the two-cigarette group (p = 0.002). The levels of sFlt-1 in the AhR antagonist group did not change regardless of two-cigarette exposure (p = 0.064). With the AhR agonist, sFlt-1 decreased significantly compared to the control (p = 0.001) and AhR antagonist group (p = 0.002). The sFlt-1 level was significantly decreased after the injection of the AhR agonist compared to the control group (p = 0.001). Serum levels of VEGF were significantly decreased in the one-cigarette-exposed group compared to the control group; however, there was no difference between the control and the two-cigarette-exposed groups. The placental expression of sFlt-1, VEGF, and sEng were inconsistent. This study offers insights into the potential role of AhR on antiangiogenic sFlt-1 associated with preeclampsia. It may support the invention of a new treatment strategy for preeclampsia using AhR activation.
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