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Updated: Jan 9, 2026
Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube SWCNT-delivered MALAT1 Antisense Oligos
Published on: December 13, 2018
A novel link between enhanced chenodeoxycholic acid synthesis and multi-walled carbon nanotubes-induced proliferation
Yunxia Liang1, Yang Zhou2, Dongli Xie1
1College of Textile and Clothing Engineering, Soochow University, 199 Ren-Ai Road, Suzhou 215123, China.
Introduction:
The increasing amount of multi-walled carbon nanotubes (MWCNTs) released into the environment due to extensive production and application has raised great concerns for public health. However, there is scarce knowledge of their detrimental effects on eyes, one organ directly exposed to the environment.
Objective:
To mine the mechanisms underlying the toxic effects of MWCNT exposure on ocular cells from the aspects of metabolomics and transcriptomics.
Methods:
Two ocular cell lines (ARPE-19 and HCE-T) were exposed to 0 or 100 μg/mL MWCNTs for 24 h and then untargeted metabolomics (n = 6) or RNA-sequencing (n = 3) were performed.
Results:
Totally, 290 differential metabolites (DMs) were identified for ARPE-19 and they were enriched in 68 KEGG pathways, while 74 DMs were obtained for HCE-T and they were annotated in 31 KEGG pathways. Venn diagrams showed 37 DMs and 20 KEGG pathways were overlapped between two cells, which comprised bile acids [e.g. chenodeoxycholic acid (CDCA)] and amino acids [e.g. leucine (Leu), glutamine (Gln)] metabolism. Totally, 3,539 and 2,005 differentially expressed genes (DEGs) were respectively screened for ARPE-19 and HCE-T, from which 70 DEGs were shared, including bile acids (CYP7B1, ABCG2)-, Gln metabolism (SLC1A5)- and inflammation (IL11, CXCL8)-related genes. Targeted metabolomics or ELISA assay confirmed CDCA, Leu and Gln were elevated in two ocular cells after MWCNT exposure, while qRT-PCR or ELISA verified MWCNT exposure up-regulated CYP7A1 and ABCG2 at protein levels, CYP7B1, BCAT1 (a hydrolytic enzyme for Leu) and SLC1A5 at mRNA and protein levels in both cells. CCK-8 assays only validated the addition of CDCA at MWCNT-induced dose reduced the cell viability and induced the expression of pro-apoptotic CASP3 as well as pro-inflammatory CXCL8 or IL11.
Conclusion:
CDCA and its related genes may represent potential targets for the diagnosis and treatment of ocular damages for populations exposed to MWCNTs.
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