Maternal exposure to environmental DEHP exacerbated OVA-induced asthmatic responses in rat offspring

Wang, Bohan; Liu, Fangwei; Dong, Jing; You, Mingdan; Fu, Yuanyuan; Li, Chao; Lu, Yiping; Chen, Jie

doi:10.1016/j.scitotenv.2017.09.276

Cited by 33 publications

(14 citation statements)

References 63 publications

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“…Moreover, adverse effects of perinatal environmental exposures may not manifest until subsequent challenges later in life, such as hormonal stimulation, poor diet, or additional environmental exposures. 65 - 67 Further studies are necessary to determine the consequences of developmental DEHP exposure on cardiac function and the potential role for DNAm in mediating these effects.…”

Section: Discussionmentioning

confidence: 99%

Sex-Specific Programming of Cardiac DNA Methylation by Developmental Phthalate Exposure

et al. 2020

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Phthalate plasticizers are ubiquitous chemicals linked to several cardiovascular diseases in animal models and humans. Despite this, the mechanisms by which phthalate exposures cause adverse cardiac health outcomes are unclear. In particular, whether phthalate exposures during pregnancy interfere with normal developmental programming of the cardiovascular system, and the resulting implications this may have for long-term disease risk, are unknown. Recent studies suggest that the effects of phthalates on metabolic and neurobehavioral outcomes are sex-specific. However, the influence of sex on cardiac susceptibility to phthalate exposures has not been investigated. One mechanism by which developmental exposures may influence long-term health is through altered programming of DNA methylation. In this work, we utilized an established mouse model of human-relevant perinatal exposure and enhanced reduced representation bisulfite sequencing to investigate the long-term effects of diethylhexyl phthalate (DEHP) exposure on DNA methylation in the hearts of adult male and female offspring at 5 months of age (n = 5-7 mice per sex and exposure). Perinatal DEHP exposure led to hundreds of sex-specific, differentially methylated cytosines (DMCs) and differentially methylated regions (DMRs) in the heart. Pathway analysis of DMCs revealed enrichment for several pathways in females, including insulin signaling, regulation of histone methylation, and tyrosine phosphatase activity. In males, DMCs were enriched for glucose transport, energy generation, and developmental programs. Notably, many sex-specific genes differentially methylated with DEHP exposure in our mouse model were also differentially methylated in published data of heart tissues collected from human heart failure patients. Together, these data highlight the potential role for DNA methylation in DEHP-induced cardiac effects and emphasize the importance of sex as a biological variable in environmental health studies.

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Section: Discussionmentioning

confidence: 99%

Sex-Specific Programming of Cardiac DNA Methylation by Developmental Phthalate Exposure

et al. 2020

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“…Previous study reported that DEHP exposure induces colon tumor promotion in rats (Chen et al, 2017). The pulmonary inflammation in rat offspring were exacerbated when pregnant or lactating rats were exposed to DEHP with the increased inflammatory factor IL-4 (Wang et al, 2018). Thus, our data suggest that DEHP-induced colonic injury could be related with oxidative stress and inflammatory response in the colon.…”

Section: Discussionmentioning

confidence: 99%

Lactobacillus plantarum TW1-1 Alleviates Diethylhexylphthalate-Induced Testicular Damage in Mice by Modulating Gut Microbiota and Decreasing Inflammation

Tian

Feng

et al. 2019

Front. Cell. Infect. Microbiol.

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Diethylhexylphthalate (DEHP), acting as an endocrine disruptor, disturbed reproductive health. Here, we evaluated the effects of Lactobacillus plantarum TW1-1 ( L. plantarum TW1-1) on DEHP-induced testicular damage in adult male mice. Results showed that oral supplementation of L. plantarum TW1-1 significantly increased the serum testosterone concentration, enhanced the semen quality, and attenuated gonad development defects in DEHP-exposed mice. L. plantarum TW1-1 also alleviated DEHP-induced oxidative stress and inflammatory responses by decreasing the mRNA expression and serum protein concentration of different inflammatory factors [tumor necrosis factor-α, interleukin (IL)-1β and IL-6]. Furthermore, L. plantarum TW1-1 significantly reduced DEHP-induced intestinal hyper-permeability and the increase in the serum lipopolysaccharide level. Gut microbiota diversity analysis revealed that L. plantarum TW1-1 shifted the DEHP-disrupted gut microbiota to that of the control mice. At phylum level, L. plantarum TW1-1 reversed DEHP-induced Bacteroidetes increase and Firmicutes decrease, and restored Deferribacteres in DEHP-exposed mice. Spearman's correlation analysis showed that Bacteroidetes, Deferribacteres , and Firmicutes were associated with DEHP-induced testicular damage. In addition, the ratio of Firmicutes to Bacteroidetes (Firm/Bac ratio) significantly decreased from 0.28 (control group) to 0.13 (DEHP-exposed group), which was restored by L. plantarum TW1-1 treatment. Correlation analysis showed that the Firm/Bac ratio was negatively correlated with testicular damage and inflammation. These findings suggest that L. plantarum TW1-1 prevents DEHP-induced testicular damage via modulating gut microbiota and decreasing inflammation.

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“…The protein concentration was measured using a BCA Kit (Thermo Scientific, Rockford, IL, United States). The process of western blot refers to previous studies ( Wang et al, 2017 ). In short, after electrophoresis, transferring to the PVDF membrane, and blocking with skim milk, membranes were incubated overnight at 4°C with primary rabbit anti-phospho-MAP2 (Ser136) (#4541, Cell Signaling Technology; 1:500), rabbit antibody anti-MAP2 (#8707, Cell Signaling Technology; 1:500), rabbit antibody anti-phospho-stathmin (Ser38) (#4191, Cell Signaling Technology, 1:500), rabbit antibody anti-stathmin (ab2906, Abcam, 1:5000), rabbit antibody anti-JNK1 (ab110724, Abcam, 1:500), rabbit antibody anti-phospho-JNK1 (Thr183) (ab47337, Abcam, 1:500), and rabbit antibody anti-β-actin (#4970, Cell Signaling Technology; 1:500).…”

Section: Methodsmentioning

confidence: 99%

“…Environmental PAEs directly or indirectly enter the human body to adversely impact human health ( Sui et al, 2014 ). As environmental endocrine-disrupting chemicals, PAEs exert pleiotropic deleterious effects on the immune, reproductive, cardiovascular, and nervous systems ( Heudorf et al, 2007 ; Zarean et al, 2016 ; Wang et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Exposure to Di-(2-ethylhexyl) Phthalate During Perinatal Period Gender-Specifically Impairs the Dendritic Growth of Pyramidal Neurons in Rat Offspring

You

Dong

et al. 2018

Front. Neurosci.

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Di-(2-ethylhexyl) phthalate (DEHP), as a prevalent xenoestrogen endocrine disrupter, is omnipresent in the environment and commonly used in polyethylene plastic products. Although DEHP has potential adverse effects on multisystem organs, damage to the central nervous system is more significant. However, the consequences and mechanisms of DEHP exposure remain to be explored. The aim of this study was to investigate the effects and related mechanisms of maternal DEHP exposure on dendritic development of hippocampal pyramidal neurons in a rat model. Pregnant Wistar rats were intragastrically administrated either vehicle or DEHP (30, 300, and 750 mg/kg/d) from gestation day 0 to postnatal day (PN) 21. The dendritic length and complexity of dendritic arbors’ pattern in pyramidal neurons of the hippocampus were measured using Golgi–Cox staining and Sholl analysis. The expression of dendritic development-related proteins was detected using western blot and immunofluorescence staining. DEHP-treated male but not female pups showed an obvious decrease in the total length and branching numbers of basal dendrites on PN7, PN14, and PN21. The phosphorylation of MAP2c, stathmin, and JNK1 in the male pup hippocampus was significantly decreased in DEHP treatment groups compared to controls. However, protein expression alteration in the hippocampus of female offspring was not observed. In summary, our study indicated that DEHP has a gender-specific negative impact on the dendritic growth of CA1 pyramidal neurons in male offspring of a rat model of DEHP exposure. The adverse impact may be related to the dysregulation of phosphorylated and total MAP2c and stathmin mediated by JNK1.

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Maternal exposure to environmental DEHP exacerbated OVA-induced asthmatic responses in rat offspring

Cited by 33 publications

References 63 publications

Sex-Specific Programming of Cardiac DNA Methylation by Developmental Phthalate Exposure

Sex-Specific Programming of Cardiac DNA Methylation by Developmental Phthalate Exposure

Lactobacillus plantarum TW1-1 Alleviates Diethylhexylphthalate-Induced Testicular Damage in Mice by Modulating Gut Microbiota and Decreasing Inflammation

Exposure to Di-(2-ethylhexyl) Phthalate During Perinatal Period Gender-Specifically Impairs the Dendritic Growth of Pyramidal Neurons in Rat Offspring

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