PCB 126 induces monocyte/macrophage polarization and inflammation through AhR and NF-κB pathways

Wang, Chunyan; Petriello, Michael C.; Zhu, Beibei; Hennig, Bernhard

doi:10.1016/j.taap.2019.02.006

Cited by 74 publications

(46 citation statements)

References 57 publications

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“…The mechanism of TCDD- and PCB-induced atherosclerosis has been well characterized by many studies [ 21 , 23 , 39 , 40 ]. Emerging data continue to demonstrate the participation of miRNAs in atherosclerosis [ 41 – 43 ] and in biological responses induced by environmental pollutants [ 44 – 46 ].…”

Section: Discussionmentioning

confidence: 99%

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and Polychlorinated Biphenyl Coexposure Alters the Expression Profile of MicroRNAs in the Liver Associated with Atherosclerosis

Shan

Chen

2020

BioMed Research International

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MicroRNAs (miRNAs) are a class of small RNAs that regulate gene expression. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and polychlorinated biphenyls (PCBs) are persistent organic pollutants that exist as complex mixtures in vivo. When humans are simultaneously exposed to these compounds, the development of atherosclerosis is known to be enhanced. However, the roles of miRNA in TCDD- and PCB-induced atherosclerosis are largely unknown. Therefore, the present study is aimed at elucidating the possible dysregulation of miRNAs in atherogenesis induced by coexposure to TCDD and PCBs. Eight-week-old male ApoE-/- mice were coexposed to TCDD (15 μg/kg) and Aroclor1254 (55 mg/kg, a representative mixture of PCBs) by intraperitoneal injection four times over a 6-week period. Microarray analysis of miRNAs and mRNAs in the liver of ApoE-/- mice with or without TCDD and Aroclor1254 coexposure was performed. We discovered that 68 miRNAs and 1312 mRNAs exhibited significant expression changes in response to TCDD and PCB coexposure and revealed that both changed miRNAs and mRNAs are involved in cardiovascular disease processes. An integrated miRNA-mRNA approach indicated that miRNA-26a-5p, miRNA-193a-3p, and miRNA-30c-5p participated in specific TCDD and Aroclor1254 coresponsive networks which are relevant to the cardiovascular system development and function network. Furthermore, our results also indicated that miRNA-130a-3p and miRNA-376a-3p were novel players in the regulation of TCDD- and Aroclor1254-induced atherosclerosis pathways. In summary, our finding provided new insights into the mechanism of atherosclerosis in response to TCDD and PCB coexposure.

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Section: Discussionmentioning

confidence: 99%

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and Polychlorinated Biphenyl Coexposure Alters the Expression Profile of MicroRNAs in the Liver Associated with Atherosclerosis

Shan

Chen

2020

BioMed Research International

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“…Developmental PCB exposures have been linked to disruptions in the microbiome and intestinal physiology [222], liver function [223,224], lipid metabolism [225], and systemic inflammation [226,227]. These outcomes overlap with comorbidities common in ASD [1], raising the question of whether developmental PCB exposures contribute to ASD comorbidities.…”

Section: A Role For Pcbs In Asd Comorbidities?mentioning

confidence: 99%

Polychlorinated Biphenyls (PCBs): Risk Factors for Autism Spectrum Disorder?

Panesar

Kennedy

Stietz

et al. 2020

Toxics

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Autism spectrum disorder (ASD) includes a group of multifactorial neurodevelopmental disorders defined clinically by core deficits in social reciprocity and communication, restrictive interests and repetitive behaviors. ASD affects one in 54 children in the United States, one in 89 children in Europe, and one in 277 children in Asia, with an estimated worldwide prevalence of 1–2%. While there is increasing consensus that ASD results from complex gene x environment interactions, the identity of specific environmental risk factors and the mechanisms by which environmental and genetic factors interact to determine individual risk remain critical gaps in our understanding of ASD etiology. Polychlorinated biphenyls (PCBs) are ubiquitous environmental contaminants that have been linked to altered neurodevelopment in humans. Preclinical studies demonstrate that PCBs modulate signaling pathways implicated in ASD and phenocopy the effects of ASD risk genes on critical morphometric determinants of neuronal connectivity, such as dendritic arborization. Here, we review human and experimental evidence identifying PCBs as potential risk factors for ASD and discuss the potential for PCBs to influence not only core symptoms of ASD, but also comorbidities commonly associated with ASD, via effects on the central and peripheral nervous systems, and/or peripheral target tissues, using bladder dysfunction as an example. We also discuss critical data gaps in the literature implicating PCBs as ASD risk factors. Unlike genetic factors, which are currently irreversible, environmental factors are modifiable risks. Therefore, data confirming PCBs as risk factors for ASD may suggest rational approaches for the primary prevention of ASD in genetically susceptible individuals.

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“…M2 macrophage secretes high level of IL-10 and TGF-β. Its role is immune suppression, tissue repair and functional remodeling (36). Much evidence demonstrated that miRNA level varied in different macrophage polarization.…”

Section: Discussionmentioning

confidence: 99%

Propofol inhibits inflammatory response by regulating the miR-494/ Nrdp1 pathway in ICH mice model

Liu

Shi

et al. 2020

Preprint

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Background: Propofol is an anesthetic agent with neuro-protective effect in neuronal injury. However, the mechanism of propofol in M1 macrophage polarization following ICH has not been well studied. Ubiquitination mediated M1/M2 macrophage polarization plays important roles in pathogenesis of immune disease. The experiment analyzed anti-inflammatory effects of propofol in macrophages following ICH. Methods: In the experiment, macrophages were administrated with erythrocyte lysates, and then miR-494, Nrdp1 and M1 related markers were analyzed. In addition, brain inflammatory response, brain edema, and neurological functions of ICH mice were also assessed. Results: We found that propofol decreased miR-494 levels while increased Nrdp1 levels in macrophages after ICH. We also demonstrated that miR-494 inhibited Nrdp1 expression by directly binding its 3′-untranslated region. MiR-494 attenuated Nrdp1 levels and downstream proinflammatory factors production. Upregulation of Nrdp1 in macrophages significantly decreased M1 macrophage polarization. Conclusion: Taken together, these results suggest that propofol can attenuate the neuroinflammatory response of macrophages after ICH through regulation of the miR-494/Nrdp1 pathway.

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PCB 126 induces monocyte/macrophage polarization and inflammation through AhR and NF-κB pathways

Cited by 74 publications

References 57 publications

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and Polychlorinated Biphenyl Coexposure Alters the Expression Profile of MicroRNAs in the Liver Associated with Atherosclerosis

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and Polychlorinated Biphenyl Coexposure Alters the Expression Profile of MicroRNAs in the Liver Associated with Atherosclerosis

Polychlorinated Biphenyls (PCBs): Risk Factors for Autism Spectrum Disorder?

Propofol inhibits inflammatory response by regulating the miR-494/ Nrdp1 pathway in ICH mice model

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