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Role of Hepatocyte- and Macrophage-Specific PPARγ in Hepatotoxicity Induced by Diethylhexyl Phthalate in Mice.
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- Author(s): Miao Xu1,2; Yongning Li1; Xiaohong Wang1; Qiannan Zhang1; Lei Wang3; Xin Zhang1; Wenming Cui1; Xiaomin Han1; Ning Ma1; Haishan Li4; Hongyun Fang5; Song Tang6,7; Jingguang Li1; Zhaoping Liu1; Hui Yang1 ; Xudong Jia1
- Source:
Environmental Health Perspectives. Jan2022, Vol. 130 Issue 1, p017005-1-017005-17. 17p. 6 Color Photographs, 1 Black and White Photograph, 2 Diagrams.- Subject Terms:
*Biochemistry; *Animal experimentation; *Plasticizers; RNA metabolism; Lipid metabolism; Hepatotoxicology -- Risk factors; Triglycerides; Flow cytometry; Cytokines; Sequence analysis; In vivo studies; Metabolomics; Fatty liver; Macrophages; Peroxisome proliferator-activated receptors; Risk assessment; Comparative studies; Dose-effect relationship in pharmacology; Liver cells; Molecular structure; Cell lines; Computer-assisted molecular modeling; Mice; Evaluation - Source:
- Additional Information
- Abstract: BACKGROUND: Phthalates may disturb metabolic homeostasis in the liver by interfering with the peroxisome proliferator-activated receptors (PPARs). However, the role of hepatic macrophages in the lipid metabolic dysregulation induced by diethylhexyl phthalate (DEHP) remains unclear. OBJECTIVES: We aimed to evaluate the respective role of hepatocyte- and macrophage-specific PPARγ in the hepatotoxicity induced by DEHP. METHODS: Wild-type (WT), hepatocyte-specific PPARγ knockout (Hep-KO), and macrophage-specific PPAR knockout (Mac-KO) mice were administered DEHP (625 mg/kg body weight) by daily gavage for 28 d, followed by hepatotoxicity examination and macrophage analysis. RNA sequencing and lipid metabolomic analysis were used to characterize the molecular changes in mouse liver. Mouse bone marrow-derived macrophages (BMDMs) and human monocytic THP-1 cell-derived macrophages were used to investigate the mechanistic regulation of macrophages’ polarization by DEHP and mono(2-ethylhexyl) phthalate (MEHP). RESULTS: The levels of hepatic steatosis and triglyceride were significantly higher in the mice treated with DEHP compared with the control mice in the WT and Hep-KO model. Lipid accumulation induced by DEHP was notably attenuated in the Mac-KO mice, but M2-polarization of hepatic macrophages in the Mac-KO mice was significantly higher compared with the WT mice under DEHP treatment. The M2-polarization of BMDMs and human macrophages was suppressed by DEHP and MEHP. Transcriptomic and lipidomic data suggested lower levels of lipid biosynthesis, fatty acid oxidation, and oxidative phosphorylation in the Mac-KO mice compared with the WT and Hep-KO mice under DEHP treatment. CONCLUSIONS: Our data suggested that the orchestrated activation of PPARα and PPARγ by MEHP may reprogram hepatic macrophages’ polarization, thereby affecting lipid homeostasis in the mouse liver. Although this conclusion was based on studies conducted in mice and in vitro, these findings may aid in elucidating the health effect of environmental phthalate exposure. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Environmental Health Perspectives is the property of National Institute of Environmental Health Sciences and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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