Abstract
BackgroundThe 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.ResultsExposure 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.ConclusionsExposure 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.
Highlights
The response of organisms to nanoplastic exposure has gradually received the attention
We further provide the evidence to indicate the role of Jun N-terminal kinase (JNK) Mitogen-activated protein kinase (MAPK) signaling in modulating the TBH-1-mediated octopamine signal and the CAT-2-mediated dopamine signal in nanopolystyrene-exposed nematodes (Fig. 3 and Additional file 1: Figure S5), which supported the function of neuronal JNK MAPK signaling raised above
We here employed C. elegans as an animal model to investigate the role of neuronal JNK MAPK signaling in response to nanopolystyrene and the underlying mechanism
Summary
The response of organisms to nanoplastic exposure has gradually received the attention. 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. The ecotoxicity at various aspects of nanopolystyrene exposure has been detected in different environmental. Caenorhabditis elegans has been shown to be highly sensitive to the toxicity of environmental toxicants or stresses [19,20,21]. Caenorhabditis elegans is useful for detecting the potential toxicity of nanopolystyrene (100 nm) at predicted environmental concentration [31, 32]. The roles of molecular signals in other tissues (such as neurons) in response to the nanopolystyrene are still largely unclear
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