Polychlorinated biphenyl exposure alters the expression profile of microRNAs associated with vascular diseases

Wahlang, Banrida; Petriello, Michael C.; Perkins, Jordan T.; Shen, Shu; Hennig, Bernhard

doi:10.1016/j.tiv.2016.06.001

Cited by 38 publications

(27 citation statements)

References 44 publications

(49 reference statements)

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“…Lastly, it is also known that PCBs induce NF-jB activation that can lead to significant increase in inflammatory agent mRNA and protein expression (Eske et al 2014). In vitro and in vivo studies showed that POPs (which could include PCBs) trigger secretion of pro-inflammatory cytokines and alter lymphocyte functionin part, via disruption of T-cell receptor (TCR) signaling and cytokine production (Imbeault et al 2012;Wahlang et al 2016;Rousselet et al 2017). In many cases, induced increases in local levels of inflammatory agents (including cytokines such as tumor necrosis factor [TNF]-a, interferon [IFN]-c, interleukin [IL]-1b and IL-2, and reactive intermediates generated by local immune cells, etc.)…”

Section: Discussionmentioning

confidence: 99%

Effects of quercetin on Aroclor 1254-induced expression of CYP₄₅₀ and cytokines in pregnant rats

Guo

et al. 2019

Journal of Immunotoxicology

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The present study aimed to investigate the protective effect of quercetin on polychlorinated biphenyls (PCB)-induced liver and embryo damage in pregnant Sprague-Dawley rats. Pregnant rats were divided into five groups, and then were orally gavaged daily with peanut oil (vehicle) or a commercial PCB mixture (Aroclor 1254)with or without co-treatment with 75, 150, or 300 mg/kg quercetinon gestation days (GD) 4-7. At GD 9, all rats were euthanized, and their blood, liver, and uterus were collected. Expressions of CYP 450 mRNA and protein in liver, cytokines (IFNc, IL-2, IL-4, and IL-6) and IFNc/IL-4 ratios in liver and sera, liver morphology, and the status of implanted embryos were analyzed. The results showed Aroclor 1254 treatment alone caused hepatic cord damage (i.e. cell disorganization, swelling, decreased cytoplasm, vacuolization), and that quercetin co-treatment appeared to mitigate this damage. Similarly, levels of CYP1A1 and CYP2B1 mRNA in livers of Aroclor 1254-only-treated rats were significantly higher than those in rats co-treated with quercetin. Hepatic and sera levels of IFNc, IL-2, IL-6, and IFNc/IL-4 ratios, and the ratio of delayed-development embryos, all increased in Aroclor 1254-treated rats, but were relatively decreased as a result of quercetin co-treatments. IL-4 levels were decreased by Aroclor 1254 and tended to increase back to normal when quercetin was used. The results indicated that quercetin imparted a protective effect against Aroclor 1254-induced toxicity in pregnant rats, in part, by modulating levels of important pro-inflammatory cytokines and reducing induced CYP1A1 and CYP2B1 expression.

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Section: Discussionmentioning

confidence: 99%

Effects of quercetin on Aroclor 1254-induced expression of CYP₄₅₀ and cytokines in pregnant rats

Guo

et al. 2019

Journal of Immunotoxicology

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“…However, data on which miRNAs are affected after exposure to environmental chemicals, such as PCBs, are still scarce. To date only two studies have looked at the effect of PCBs on miRNA expression profiles; Zhu et al (2012) demonstrated differential expression of miRNAs in PCB exposed P19 cells in cardiac myocytes, and Wahlang et al (2016) have found that PCBs alter the expression profile of miRNAs associated with vascular disease. No studies have yet determined the effect of PCBs on any immune associated miRNAs, including miR‐155.…”

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confidence: 99%

Deregulation of microRNA‐155 and its transcription factor NF‐kB by polychlorinated biphenyls during viral infections

Waugh

Arukwe

Jaspers

2018

APMIS

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Polychlorinated biphenyls (PCBs), and similar environmental contaminants, have been linked to virus outbreaks and increased viral induced mortality since the 1970s. Yet the mechanisms behind this increased susceptibility remain elusive. It has recently been illustrated that the innate immune viral detection system is tightly regulated by small non-coding RNAs, including microRNAs (miRNAs). For virus infections miRNA-155 expression is an important host response against infection, and deregulation of this miRNA is closely associated with adverse outcomes. Thus, we designed a targeted in vitro study using primary chicken fibroblasts, first exposed to a mixture of PCBs (Arochlor-1250) before being stimulated with a synthetic RNA virus (poly I:C), to determine if PCBs have the potential to deregulate miRNA-155. In this paper, we provide the first data for the deregulation of miRNA-155 when a host is exposed to a mixture of PCBs before a virus infection. Thus, we provide important evidence that PCBs can be involved in the deregulation of important miRNA pathways involved in the immune system; thereby demonstrating novel insights into the mechanism of PCB toxicity on the immune system.

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“…It has been consistently demonstrated that exposure to environmental pollutants can influence epigenetic modifications (65–69). Specifically, exposure to persistent organic pollutants can alter the epigenetic code through several mechanisms.…”

Section: Epigenetics As An Emerging Area Of Pollutant Toxicity Rmentioning

confidence: 99%

“…For example, we have demonstrated that exposure to coplanar PCBs, including PCB 77 and PCB126, can induce vascular endothelial cell dysfunction and inflammation through alterations in histone modifications of the p65 subunit of NF-kB that result in its increased activation (66). Additionally, we have shown that the commercial PCB mixture Aroclor 1260 can upregulate miRNAs associated with cardiac injury and inflammatory pathways in primary human endothelial cells (69). In humans, it has been observed that exposure to polyaromatic hydrocarbons (PAH) results in alterations in specific miRNAs associated with oxidative DNA damage and lipid peroxidation in coke oven workers (67).…”

Section: Epigenetics As An Emerging Area Of Pollutant Toxicity Rmentioning

confidence: 99%

Impact of nutrition on pollutant toxicity: an update with new insights into epigenetic regulation

Hoffman

Petriello

Hennig

2017

Reviews on Environmental Health

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Abstract Exposure to environmental pollutants is a global health problem and is associated with the development of many chronic diseases, including cardiovascular disease, diabetes and metabolic syndrome. There is a growing body of evidence that nutrition can both positively and negatively modulate the toxic effects of pollutant exposure. Diets high in proinflammatory fats, such as linoleic acid, can exacerbate pollutant toxicity, whereas diets rich in bioactive and anti-inflammatory food components, including omega-3 fatty acids and polyphenols, can attenuate toxicant-associated inflammation. Previously, researchers have elucidated direct mechanisms of nutritional modulation, including alteration of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling, but recently, increased focus has been given to the ways in which nutrition and pollutants affect epigenetics. Nutrition has been demonstrated to modulate epigenetic markers that have been linked either to increased disease risks or to protection against diseases. Overnutrition (i.e. obesity) and undernutrition (i.e. famine) have been observed to alter prenatal epigenetic tags that may increase the risk of offspring developing disease later in life. Conversely, bioactive food components, including curcumin, have been shown to alter epigenetic markers that suppress the activation of NF-κB, thus reducing inflammatory responses. Exposure to pollutants also alters epigenetic markers and may contribute to inflammation and disease. It has been demonstrated that pollutants, via epigenetic modulations, can increase the activation of NF-κB and upregulate microRNAs associated with inflammation, cardiac injury and oxidative damage. Importantly, recent evidence suggests that nutritional components, including epigallocatechin gallate (EGCG), can protect against pollutant-induced inflammation through epigenetic regulation of proinflammatory target genes of NF-κB. Further research is needed to better understand how nutrition can modulate pollutant toxicity through epigenetic regulation. Therefore, the objective of this review is to elucidate the current evidence linking epigenetic changes to pollutant-induced diseases and how this regulation may be modulated by nutrients allowing for the development of future personalized lifestyle interventions.

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Polychlorinated biphenyl exposure alters the expression profile of microRNAs associated with vascular diseases

Cited by 38 publications

References 44 publications

Effects of quercetin on Aroclor 1254-induced expression of CYP₄₅₀ and cytokines in pregnant rats

Effects of quercetin on Aroclor 1254-induced expression of CYP₄₅₀ and cytokines in pregnant rats

Deregulation of microRNA‐155 and its transcription factor NF‐kB by polychlorinated biphenyls during viral infections

Impact of nutrition on pollutant toxicity: an update with new insights into epigenetic regulation

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Polychlorinated biphenyl exposure alters the expression profile of microRNAs associated with vascular diseases

Cited by 38 publications

References 44 publications

Effects of quercetin on Aroclor 1254-induced expression of CYP450 and cytokines in pregnant rats

Effects of quercetin on Aroclor 1254-induced expression of CYP450 and cytokines in pregnant rats

Deregulation of microRNA‐155 and its transcription factor NF‐kB by polychlorinated biphenyls during viral infections

Impact of nutrition on pollutant toxicity: an update with new insights into epigenetic regulation

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Product

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Effects of quercetin on Aroclor 1254-induced expression of CYP₄₅₀ and cytokines in pregnant rats

Effects of quercetin on Aroclor 1254-induced expression of CYP₄₅₀ and cytokines in pregnant rats