Sharareh Ameli’s research while affiliated with Vanderbilt University and other places

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Publications (5)


Corrigendum: The potential relationship between environmental endocrine disruptor exposure and the development of endometriosis and adenomyosis
  • Article
  • Full-text available

August 2023

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32 Reads

Victoria R. Stephens

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Sharareh Ameli

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[...]

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[This corrects the article DOI: 10.3389/fphys.2021.807685.].

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Figure 3. A paternal fish oil diet preconception reduced toxicant-driven pulmonary Cxcr2 gene expression in F2 TCDD pups. Lung RNA was isolated from all groups and subjected to qRT-PCR to measure Cxcr2 mRNA expression. For this set of experiments, each exposure and treatment group consisted of 3 pups from different litters. (** p < 0.01, *** p < 0.001).
Figure 6. Impact of paternal and neonatal exposures and risk of pulmonary fibrosis. Representative images from multiple lungs (N = 3/group) of Masson's Trichrome-stained perfused lung tissue on postnatal day 11. Original magnification 200× (A-D,I-L) and 400× (E-H,M-P). F2 NONE (A,E), F2 NONE /Form (B,F), F2 NONE /Fish (C,G), F2 NONE /Fish/Form (D,H), F2 TCDD (I,M), F2 TCDD / Form (J,N), F2 TCDD /Fish ( K,O), F2 TCDD /Fish/Form (L,P).
Description of pup nomenclature used throughout the manuscript.
A Paternal Fish Oil Diet Preconception Reduces Lung Inflammation in a Toxicant-Driven Murine Model of New Bronchopulmonary Dysplasia

February 2023

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43 Reads

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3 Citations

Marine Drugs

New bronchopulmonary dysplasia (BPD) is a neonatal disease that is theorized to begin in utero and manifests as reduced alveolarization due to inflammation of the lung. Risk factors for new BPD in human infants include intrauterine growth restriction (IUGR), premature birth (PTB) and formula feeding. Using a mouse model, our group recently reported that a paternal history of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure increased his offspring’s risk of IUGR, PTB, and new BPD. Additionally, formula supplementation of these neonates worsened the severity of pulmonary disease. In a separate study, we reported that a paternal preconception fish oil diet prevented TCDD-driven IUGR and PTB. Not surprisingly, eliminating these two major risk factors for new BPD also significantly reduced development of neonatal lung disease. However, this prior study did not examine the potential mechanism for fish oil’s protective effect. Herein, we sought to determine whether a paternal preconception fish oil diet attenuated toxicant-associated lung inflammation, which is an important contributor to the pathogenesis of new BPD. Compared to offspring of standard diet TCDD-exposed males, offspring of TCDD-exposed males provided a fish oil diet prior to conception exhibited a significant reduction in pulmonary expression of multiple pro-inflammatory mediators (Tlr4, Cxcr2, Il-1 alpha). Additionally, neonatal lungs of pups born to fish oil treated fathers exhibited minimal hemorrhaging or edema. Currently, prevention of BPD is largely focused on maternal strategies to improve health (e.g., smoking cessation) or reduce risk of PTB (e.g., progesterone supplementation). Our studies in mice support a role for also targeting paternal factors to improve pregnancy outcomes and child health.


Figure 4. A paternal fish oil diet preconception influences Negativicutes orders in the intestines of F2CT pups: (A) Bar graphs represent the relative abundance of Negativicutes, (B) Veillonellaceae, and (C) Selenomondales in the colon content of offspring. Data analyzed using one-way ANOVA and the Tukey Post Hoc Test; Data represent the mean +/− SD from 3 non-littermates *** p ≤ 0.001, **** p ≤ 0.0001.
Description of pup nomenclature used throughout the manuscript.
A paternal fish oil diet preconception reduces the incidence of NEC in offspring.
A Paternal Fish Oil Diet Preconception Modulates the Gut Microbiome and Attenuates Necrotizing Enterocolitis in Neonatal Mice

June 2022

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36 Reads

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6 Citations

Marine Drugs

Epidemiology and animal studies suggest that a paternal history of toxicant exposure contributes to the developmental origins of health and disease. Using a mouse model, our laboratory previously reported that a paternal history of in utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) increased his offspring’s risk of developing necrotizing enterocolitis (NEC). Additionally, our group and others have found that formula supplementation also increases the risk of NEC in both humans and mice. Our murine studies revealed that intervening with a paternal fish oil diet preconception eliminated the TCDD-associated outcomes that are risk factors for NEC (e.g., intrauterine growth restriction, delayed postnatal growth, and preterm birth). However, the efficacy of a paternal fish oil diet in eliminating the risk of disease development in his offspring was not investigated. Herein, reproductive-age male mice exposed to TCDD in utero were weaned to a standard or fish oil diet for one full cycle of spermatogenesis, then mated to age-matched unexposed females. Their offspring were randomized to a strict maternal milk diet or a supplemental formula diet from postnatal days 7–10. Offspring colon contents and intestines were collected to determine the onset of gut dysbiosis and NEC. We found that a paternal fish oil diet preconception reduced his offspring’s risk of toxicant-driven NEC, which was associated with a decrease in the relative abundance of the Firmicutes phylum, but an increase in the relative abundance of the Negativicutes class.


Endometriosis and adenomyosis exhibit overlapping phenotypes. Adenomyosis has been referred to as “endometriosis interna” due to its resemblance to endometriosis both histologically and phenotypically. However, as shown in the Venn diagram, while the diseases have many common features, they also exhibit a number of differences. Created with BioRender.com.
Potential mechanisms by which developmental exposure to environmental endocrine disruptors may induce disease or dysfunction. EDCs may act as steroid agonists or antagonists by binding receptors and interfering with downstream responses. EDCs may also act via non-genomic mechanisms via binding to G-protein coupled receptors. Finally, interference with steroid action can promote inflammation via a variety of mechanisms, including the failure to curtail production of reactive oxygen species. Created with BioRender.com.
Health effects of selected endocrine disrupting chemicals.
The Potential Relationship Between Environmental Endocrine Disruptor Exposure and the Development of Endometriosis and Adenomyosis

January 2022

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200 Reads

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30 Citations

Women with endometriosis, the growth of endometrial glands and stroma outside the uterus, commonly also exhibit adenomyosis, the growth of endometrial tissues within the uterine muscle. Each disease is associated with functional alterations in the eutopic endometrium frequently leading to pain, reduced fertility, and an increased risk of adverse pregnancy outcomes. Although the precise etiology of either disease is poorly understood, evidence suggests that the presence of endometriosis may be a contributing factor to the subsequent development of adenomyosis as a consequence of an altered, systemic inflammatory response. Herein, we will discuss the potential role of exposure to environmental toxicants with endocrine disrupting capabilities in the pathogenesis of both endometriosis and adenomyosis. Numerous epidemiology and experimental studies support a role for environmental endocrine disrupting chemicals (EDCs) in the development of endometriosis; however, only a few studies have examined the potential relationship between toxicant exposures and the risk of adenomyosis. Nevertheless, since women with endometriosis are also frequently found to have adenomyosis, discussion of EDC exposure and development of each of these diseases is relevant. We will discuss the potential mechanisms by which EDCs may act to promote the co-development of endometriosis and adenomyosis. Understanding the disease-promoting mechanisms of environmental toxicants related to endometriosis and adenomyosis is paramount to designing more effective treatment(s) and preventative strategies.


Figure 1. A dietary fish oil intervention improves postnatal development in pups: CT and F2TCDD pup body weight was monitored from postnatal day 7-10 (A), lung hypoplasia was determined by measuring lung-to-body weight ratios in CT and F2TCDD pups (B). Growth curve data represents the mean value of 4-5 non-littermate pups. Lung-to-body weight ratio data represents individual values of 4-5 non-littermate pups. Standard deviation is shown. *** p ≤ 0.001.
Figure 2. A paternal dietary fish oil intervention improves lung development in pups: Representative images of Hematoxylin-and Eosin-stained perfused lung tissue of PND11 CT pups sired by a standard or fish oil diet father following a maternal milk diet or supplemental formula at a magnification of 100× (A-D) and 400× (E-H); F2TCDD pups sired by a standard or fish oil diet father following a maternal milk diet or formula supplementation at a magnification of 100× (I-L) and 400× (M-P).
Figure 3. A paternal dietary fish oil intervention improves the alveolarization of pup lungs: Pulmonary alveolar space (A), mean linear intercept (B), and radial alveolar count (C) of CT and F2TCDD pups ± a fish oil intervention and/or supplemental formula was measured on PND11. Groups used for manual determination of pulmonary alveolar space and radial alveolar count contained 6-10 non-littermates. Data points represent the mean values from individual pups. Standard deviation is shown. Groups used for automated mean linear intercept contained 3-4 non-littermates.* p ≤ 0.05; ** p ≤ 0.01;*** p ≤ 0.001;**** p ≤ 0.0001.
Figure 4. A dietary fish oil intervention reduces the incidence of BPD in TCDD-exposed pups: Incidence of BPD was determined in CT and F2TCDD pups ± a fish oil intervention and/or formula supplementation (A), the incidence of BPD was determined using a novel scale based on lung histology (B-G). Data points represent the individual lung injury scores of 6-10 non-littermates from each group. Standard deviation is shown. **** p ≤ 0.0001.
Incidence of pups with BPD across all groups. CT, control; FO, fish oil.
A Preconception Paternal Fish Oil Diet Prevents Toxicant-Driven New Bronchopulmonary Dysplasia in Neonatal Mice

December 2021

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50 Reads

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4 Citations

Toxics

New bronchopulmonary dysplasia is a developmental lung disease associated with placental dysfunction and impaired alveolarization. Risk factors for new BPD include prematurity, delayed postnatal growth, the dysregulation of epithelial-to-mesenchymal transition (EMT), and parental exposure to toxicants. Our group previously reported that a history of paternal toxicant exposure increased the risk of prematurity and low birth weight in offspring. A history of paternal toxicant exposure also increased the offspring’s risk of new BPD and disease severity was increased in offspring who additionally received a supplemental formula diet, which has also been linked to poor lung development. Risk factors associated with new BPD are well-defined, but it is unclear whether the disease can be prevented. Herein, we assessed whether a paternal fish oil diet could attenuate the development of new BPD in the offspring of toxicant exposed mice, with and without neonatal formula feeding. We investigated the impact of a paternal fish oil diet preconception because we previously reported that this intervention reduces the risk of TCDD associated placental dysfunction, prematurity, and low birth weight. We found that a paternal fish oil diet significantly reduced the risk of new BPD in neonatal mice with a history of paternal toxicant exposure regardless of neonatal diet. Furthermore, our evidence suggests that the protective effects of a paternal fish oil diet are mediated in part by the modulation of small molecules involved in EMT.

Citations (4)


... A growing body of research from rodent models is shedding light on potential mechanisms through which paternal factors including dietary predilections [14,31], exposure to environmental stressors like toxicants [32], and epigenetic modifications within spermatozoa [33] can have longterm effects on offspring health. For instance, several studies using mainly rodent animal-based models have identified links between paternal diet, obesity and low sperm quality and increased risks of cardio-metabolic disorders (e.g., obesity and type 2 diabetes) in offspring [34][35][36][37]. ...

Reference:

Contribution of the seminal microbiome to paternal programming
A Paternal Fish Oil Diet Preconception Reduces Lung Inflammation in a Toxicant-Driven Murine Model of New Bronchopulmonary Dysplasia

Marine Drugs

... Another murine study showed that a paternal diet containing high fish oil before conception reduced the incidence of necrotizing enterocolitis in the offspring [47]. According to the followup study, male mice fed fish oil for one spermatogenic cycle prior to mating showed a decrease in pulmonary inflammation and respiratory pro-inflammatory cytokine expression in the pups [32]. ...

A Paternal Fish Oil Diet Preconception Modulates the Gut Microbiome and Attenuates Necrotizing Enterocolitis in Neonatal Mice

Marine Drugs

... Moreover, a recent systematic review of 50 epidemiological studies highlighted positive associations between endometriosis and several environmental contaminants, including polychlorinated biphenyls, dioxins, phthalates, organochlorines, and bisphenol A 175 . These substances may disrupt tissue homeostasis through various mechanisms, such as acting as endocrine disruptors, modulating immune function, inducing oxidative stress and perturbing epigenetic processes [176][177][178] . Consequently, such disruptions can perturb endometrial cell functions and pathways that regulate cell proliferation, differentiation, and decidualization 179,180 , leading to perturbations on the cellular and/or organ level. ...

The Potential Relationship Between Environmental Endocrine Disruptor Exposure and the Development of Endometriosis and Adenomyosis

... Since IUGR and PTB are well-known risk factors for new BPD, our group recently assessed the incidence of this disease in offspring of TCDD-exposed males (F2 TCDD mice). We demonstrated that new BPD was common in F2 TCDD pups, and that formula supplementation of these neonates heightened the severity of disease [9,10]. ...

A Preconception Paternal Fish Oil Diet Prevents Toxicant-Driven New Bronchopulmonary Dysplasia in Neonatal Mice

Toxics