Lipid metabolic response to polystyrene particles in nematode Caenorhabditis elegans

Yang, Yunhan; Shao, Huimin; Wu, Qiuli; Wang, Dayong

doi:10.1016/j.envpol.2019.113439

Cited by 74 publications

(16 citation statements)

References 53 publications

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“…So far, in the intestine, two signaling pathways (insulin and p38 MAPK signaling pathways) have been identified to be involved in the control of response to nanopolystyrene [33][34][35]54]. In the intestine, we found that the DOP-1 regulated the response to nanopolystyrene by activating the downstream signaling cascade in p38 MAPK signaling pathway (Fig.…”

Section: Discussionmentioning

confidence: 73%

“…Therefore, the alteration in genes encoding the JNK MAPK signaling pathway induced by nanopolystyrene in the range of μg/L mediated a protective response to nanopolystyrene. Similarly, the alteration in genes encoding insulin and p38 MAPK signaling pathways induced by nanopolystyrene in the range of μg/L also mediated a protective response to nanopolystyrene in nematodes [33][34][35].…”

Section: Discussionmentioning

confidence: 91%

“…In C. elegans, there are three MAPK signaling pathways (p38, JNK, and ERK signaling pathways) [21,24]. p38 MAPK signaling pathway acted in the intestine to regulate the response to nanopolystyrene in nematodes [34,35]. These observations suggest that different MAPK signaling pathways can provide the molecular basis for different tissues in response to nanopolystyrene.…”

Section: Discussionmentioning

confidence: 96%

“…In nematodes, pmk-1 encodes the p38 MAPK in p38 MAPK signaling pathway, and daf-16 encodes the FOXO transcriptional factor in insulin signaling pathway. Recently, it has been further shown that the signaling cascade of mdt-15-sbp-1 encoding the lipid metabolic signaling acted downstream of p38 MAPK signaling to regulate the response to nanopolystyrene [35]. In the intestine, we further examined the effect of RNAi knockdown of dop-1, octr-1, or ser-6 on expression of genes encoding p38 MAPK and insulin signaling pathways in nanopolystyrene-exposed nematodes.…”

Section: Effect Of Intestinal Rnai Knockdown Of Dop-1 Octr-1 or Sermentioning

confidence: 99%

“…Caenorhabditis elegans is useful for detecting the potential toxicity of nanopolystyrene (100 nm) at predicted environmental concentration [31,32]. In nematodes, some intestinal signaling pathways (such as insulin and p38 mitogen-activated protein kinase (MAPK) signaling pathways) are required for the response to nanopolystyrene [33][34][35]. Nevertheless, the roles of molecular signals in other tissues (such as neurons) in response to the nanopolystyrene are still largely unclear.…”

Section: Introductionmentioning

confidence: 99%

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Exposure to low-dose nanopolystyrene induces the response of neuronal JNK MAPK signaling pathway in nematode Caenorhabditis elegans

Zhao

et al. 2020

Environ Sci Eur

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Background: The response of organisms to nanoplastic exposure has gradually received the attention. Nevertheless, the role of neurons in response to nanoplastic exposure and the underlying mechanism are still largely unclear. We here examined the role of neuronal JNK MAPK signaling in response to low-dose of polystyrene (100 nm) in Caenorhabditis elegans. Results: Exposure to nanopolystyrene in the range of μg/L could increase the expression of genes (jkk-1, mek-1, and jnk-1) encoding JNK MAPK signaling pathway. Meanwhile, RNAi knockdown of any of these genes induced a susceptibility to nanopolystyrene toxicity. In the neurons, SNB-1/synaptobrevin was identified as the downstream target of JNK-1/JNK, suggesting the alteration in neurotransmitter signals in nanopolystyrene-exposed nematodes. In nanopolystyrene-exposed nematodes, JNK-1 modulated TBH-1-mediated octopamine signal and CAT-2-mediated dopamine signal. TBH-1 and CAT-2 further regulated the response to nanopolystyrene by affecting the function of corresponding intestinal octopamine receptors (SER-6 and OCTR-1) and intestinal dopamine receptor (DOP-1). In the intestine, DOP-1 regulated the response to nanopolystyrene by activating the downstream signaling cascade in p38 MAPK signaling pathway. Conclusions: Exposure to low-dose of nanopolystyrene could induce the response of neuronal JNK MAPK signaling pathway in nematodes. Our data further highlight the crucial role of neuronal JNK MAPK signaling-activated alteration in octopamine and dopamine signals in regulating the response to nanopolystyrene in organisms.

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Section: Discussionmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 96%

Section: Effect Of Intestinal Rnai Knockdown Of Dop-1 Octr-1 or Sermentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Exposure to low-dose nanopolystyrene induces the response of neuronal JNK MAPK signaling pathway in nematode Caenorhabditis elegans

Zhao

et al. 2020

Environ Sci Eur

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Long‐Chain Acyl Carnitines Aggravate Polystyrene Nanoplastics‐Induced Atherosclerosis by Upregulating MARCO

et al. 2023

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Exposure to micro‐ and nanoplastics (MNPs) is common because of their omnipresence in environment. Recent studies have revealed that MNPs may cause atherosclerosis, but the underlying mechanism remains unclear. To address this bottleneck, ApoE−/− mice are exposed to 2.5–250 mg kg−1 polystyrene nanoplastics (PS‐NPs, 50 nm) by oral gavage with a high‐fat diet for 19 weeks. It is found that PS‐NPs in blood and aorta of mouse exacerbate the artery stiffness and promote atherosclerotic plaque formation. PS‐NPs activate phagocytosis of M1‐macrophage in the aorta, manifesting as upregulation of macrophage receptor with collagenous structure (MARCO). Moreover, PS‐NPs disrupt lipid metabolism and increase long‐chain acyl carnitines (LCACs). LCAC accumulation is attributed to the PS‐NP‐inhibited hepatic carnitine palmitoyltransferase 2. PS‐NPs, as well as LCACs alone, aggravate lipid accumulation via upregulating MARCO in the oxidized low‐density lipoprotein‐activated foam cells. Finally, synergistic effects of PS‐NPs and LCACs on increasing total cholesterol in foam cells are found. Overall, this study indicates that LCACs aggravate PS‐NP‐induced atherosclerosis by upregulating MARCO. This study offers new insight into the mechanisms underlying MNP‐induced cardiovascular toxicity, and highlights the combined effects of MNPs with endogenous metabolites on the cardiovascular system, which warrant further study.

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Nanoplastic Toxicity: Insights and Challenges from Experimental Model Systems

Schröter

Ventura

2022

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Nanoplastic particles (NPs) can be produced or derived from the degradation of several daily used products and can therefore be found in the air, water, and food. Every day, these microscopic particles are confronted by different routes of exposure. Recent investigations have shown the internalization of these particles, differing in size and modification, in vivo in aquatic organisms and terrestrial organisms, as well as in vitro in different human cell lines. During the last years, the number of studies investigating the effects of NPs using widely different model systems and experimental approaches is exponentially growing, thus providing information about NPs, especially about polystyrene particle toxicity on health. To facilitate the grasping of the most relevant information, an overview is provided on the toxic effects of NPs coming from studies in cellular systems and in vivo in model organisms and on aspects which can be of particular relevance for particle toxicity (e.g., particle internalization mechanisms and structural modifications). Major achievements and gaps in the field as well as the point of view on how more systematic studies and exploitation of in vivo model organisms may improve the knowledge on important aspects of NPs are also pointed out.

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Lipid metabolic response to polystyrene particles in nematode Caenorhabditis elegans

Cited by 74 publications

References 53 publications

Exposure to low-dose nanopolystyrene induces the response of neuronal JNK MAPK signaling pathway in nematode Caenorhabditis elegans

Exposure to low-dose nanopolystyrene induces the response of neuronal JNK MAPK signaling pathway in nematode Caenorhabditis elegans

Long‐Chain Acyl Carnitines Aggravate Polystyrene Nanoplastics‐Induced Atherosclerosis by Upregulating MARCO

Nanoplastic Toxicity: Insights and Challenges from Experimental Model Systems

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