Nicotinamide improves the impaired extravillous trophoblast cell invasion induced by PM 2.5 exposure-associated increase of TNFα secretion through the ROS/NF-κB/FLT1 pathway.

Autor: Tao S; NHC Key Lab of Reproduction Regulation, Shanghai Engineering Research Center of Reproductive Health Drugs and Devices, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai 200237, China; Department of Pharmacy, Affiliated Children's Hospital of Jiangnan University, Wuxi, Jiangsu 214000, China. Electronic address: 18111150003@fudan.edu.cn., Zhang X; NHC Key Lab of Reproduction Regulation, Shanghai Engineering Research Center of Reproductive Health Drugs and Devices, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai 200237, China. Electronic address: xuanzhang@sibpt.com., Yang L; NHC Key Lab of Reproduction Regulation, Shanghai Engineering Research Center of Reproductive Health Drugs and Devices, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai 200237, China. Electronic address: yanglong@sibpt.com., Yang M; NHC Key Lab of Reproduction Regulation, Shanghai Engineering Research Center of Reproductive Health Drugs and Devices, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai 200237, China. Electronic address: mingjun0707@163.com., Pan B; Department of Environmental Health, School of Public Health, Fudan University, Shanghai 200032, China. Electronic address: 18211020079@fudan.edu.cn., Xu Y; Department of Environmental Health, School of Public Health, Fudan University, Shanghai 200032, China. Electronic address: yanyi_xu@fudan.edu.cn., Li W; NHC Key Lab of Reproduction Regulation, Shanghai Engineering Research Center of Reproductive Health Drugs and Devices, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai 200237, China. Electronic address: weihua.li@sibpt.com., Wang J; NHC Key Lab of Reproduction Regulation, Shanghai Engineering Research Center of Reproductive Health Drugs and Devices, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai 200237, China. Electronic address: wangjian@sibpt.com.
Jazyk: angličtina
Zdroj: Ecotoxicology and environmental safety [Ecotoxicol Environ Saf] 2024 Sep 01; Vol. 282, pp. 116733. Date of Electronic Publication: 2024 Jul 18.
DOI: 10.1016/j.ecoenv.2024.116733
Abstrakt: It has been well acknowledged that maternal exposure to fine particulate matters (PM 2.5 ) might lead to poor pregnancy outcomes including the intrauterine growth restriction (IUGR) by interfering with the placental development. Our previous studies have demonstrated that maternal PM 2.5 exposure induces IUGR, accompanied with increased maternal circulating TNFα level and impaired extravillous trophoblast cells (EVTs) invasion in mice. In this study, HTR8/SVneo cells, the immortalized human EVTs line, were used to assess effects and the underlying molecular mechanisms of nicotinamide on the impaired EVTs invasion. Our results showed that, the placental FLT1 protein level was significantly increased whereas maternal serum nicotinamide concentration was remarkably decreased in PM 2.5 -exposured pregnant mice at GD17.5 (vaginal plug day=GD0.5), compared to that in normal GD17.5 pregnant mice. FLT1 expression in HTR8/SVneo cells was significantly up-regulated by TNFα treatment, and the down-regulated FLT1 expression effectively abated the inhibitory effects of TNFα on HTR8/SVneo cells migration and invasion. Meanwhile, TNFα promoted reactive oxygen species (ROS) production and NF-κB signaling pathway activation in HTR8/SVneo cells in a dose-dependent manner. Nicotinamide treatment significantly reversed the effects of TNFα on cell migration and invasion, as well as the FLT1 expression, ROS production and NF-κB pathway activation. In summary, increased TNFα induced by PM 2.5 exposure inhibits EVTs invasion by activating the ROS/NF-κB/FLT1 signaling pathway, and this adverse effect could be attenuated by nicotinamide treatment, suggesting a potential application in the clinical intervention of PM 2.5 -induced IUGR.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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