9.C.22.  The Earthworm Coelomocyte MoS(2) Nanosheets Uptake (MoS(2)NSU) Family 

Fully understanding the cellular uptake and intracellular localization of MoS(2) nanosheets (NSMoS(2)) is a prerequisite for their safe applications. Sun et al. 2023 characterized the uptake profile of NSMoS(2) by functional coelomocytes of the earthworm Eisenia fetida. Considering that vacancy engineering is widely applied to enhance NSMoS(2) performance, they assessed the potential role of such atomic vacancies in regulating cellular uptake processes. Coelomocyte internalization and lysosomal accumulation of NSMoS(2) were tracked by fluorescent labeling imaging. Cellular uptake inhibitors, proteomics, and transcriptomics helped to mechanistically distinguish vacancy-mediated endocytosis pathways. Specifically, Mo ions activated transmembrane transporter and ion-binding pathways, entering the coelomocyte through assisted diffusion. Unlike molybdate, pristine NSMoS(2) (P-NSMoS(2)) induced protein polymerization and upregulated gene expression related to actin filament binding, which phenotypically initiated actin-mediated endocytosis. Conversely, vacancy-rich NSMoS(2) (V-NSMoS(2)) was internalized by coelomocytes through a vesicle-mediated and energy- dependent pathway. Mechanistically, atomic vacancies inhibited mitochondrial transport gene expression and likely induced membrane stress, significantly enhancing endocytosis (20.3%, p < 0.001). Molecular dynamics modeling revealed structural and conformational damage of cytoskeletal proteins caused by P-NSMoS(2), as well as the rapid response of transport protein to V-NSMoS(2). Thus, earthworm functional coelomocytes can accumulate NSMoS(2) and directly mediate cytotoxicity, and atomic vacancies can alter the endocytic pathway while enhancing cellular uptake by reprogramming protein responses and gene expression patterns. This study provides a mechanistic understanding of the ecological risks of NSMoS(2) (Sun et al. 2023).

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