Multi-walled carbon nanotubes act as a chemokine and recruit macrophages by activating the PLC/IP3/CRAC channel signaling pathway

Li, Hui; Tan, Xiaoqiu; Li, Yan; Zeng, Bo; Meng, Jie; Xu, Haiyan; Cao, Ji-Min

doi:10.1038/s41598-017-00386-3

Cited by 14 publications

(7 citation statements)

References 47 publications

(46 reference statements)

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“…Furthermore, potential changes of gene expression and other relatively slower biological processes also unlikely underlie the acute toxic effects of PtNPs, as these processes need more than 5 mins. This quick action pattern of PtNPs on cells is similar to AgNPs21 but is different from multiwalled carbon nanotubes, the latter affect cells on the intracellular side and thus is endocytosis dependent as we have reported previously 26. Another potential mechanism might be oxidative stress caused by PtNPs 27,28.…”

Section: Discussionsupporting

confidence: 62%

<p>The acute toxic effects of platinum nanoparticles on ion channels, transmembrane potentials of cardiomyocytes in vitro and heart rhythm in vivo in mice</p>

Lin¹,

Gu²,

Cao³

2019

IJN

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Background Platinum nanoparticles (PtNPs) have been considered a nontoxic nanomaterial and been clinically used in cancer chemotherapy. PtNPs can also be vehicle exhausts and environmental pollutants. These situations increase the possibility of human exposure to PtNPs. However, the potential biotoxicities of PtNPs including that on cardiac electrophysiology have been poorly understood. Methods Ion channel currents of cardiomyocytes were recorded by patch clamp. Heart rhythm was monitored by electrocardiogram recording. Morphology and characteristics of PtNPs were examined by transmission electron microscopy, dynamic light scattering and electrophoretic light scattering analyses. Results In cultured neonatal mice ventricular cardiomyocytes, PtNPs with diameters 5 nm (PtNP-5) and 70 nm (PtNP-70) concentration-dependently (10 –9 – 10 –5 g/mL) depolarized the resting potentials, suppressed the depolarization of action potentials and delayed the repolarization of action potentials. At the ion channel level, PtNPs decreased the current densities of I Na , I K1 and I to channels, but did not affect the channel activity kinetics. In vivo, PtNP-5 and PtNP-70 dose-dependently (3–10 mg/kg, i.v.) decreased the heart rate and induced complete atrioventricular conduction block (AVB) at higher doses. Both PtNP-5 and PtNP-70 (10 –9 – 10 –5 g/mL) did not significantly increase the generation of ROS and leak of lactate dehydrogenase (LDH) from cardiomyocytes within 5 mins after exposure except that only very high PtNP-5 (10 –5 g/mL) slightly increased LDH leak. The internalization of PtNP-5 and PtNP-70 did not occur within 5 mins but occurred 1 hr after exposure. Conclusion PtNP-5 and PtNP-70 have similar acute toxic effects on cardiac electrophysiology and can induce threatening cardiac conduction block. These acute electrophysiological toxicities of PtNPs are most likely caused by a nanoscale interference of PtNPs on ion channels at the extracellular side, rather than by oxidative damage or other slower biological processes.

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Section: Discussionsupporting

confidence: 62%

<p>The acute toxic effects of platinum nanoparticles on ion channels, transmembrane potentials of cardiomyocytes in vitro and heart rhythm in vivo in mice</p>

Lin¹,

Gu²,

Cao³

2019

IJN

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“…The translocation and full enzymatic activities of ALOX5 and ALOX15 require intracellular Ca 2+ signaling (62,63). MWCNTs-treated cells have been shown to have elevated intracellular Ca 2+ levels via membrane calcium channel activation (64). Additional studies are needed to identify intracellular Ca 2+ signaling activation by different types of ENMs for activation of the ALOX pathways in M1 and M2 macrophages, respectively.…”

Section: Discussionmentioning

confidence: 99%

Resolution of Pulmonary Inflammation Induced by Carbon Nanotubes and Fullerenes in Mice: Role of Macrophage Polarization

et al. 2020

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M2 macrophages resulting in increased preferential biosynthesis of proinflammatory LMs or SPMs. MWCNTs increased the M1-or M2-specific production of LMs accordingly. These findings support a mechanism by which persistent ENM-induced neutrophilic inflammation is actively resolved through time-dependent polarization of macrophages and enhanced biosynthesis of specialized LMs via distinct ALOX pathways.

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“…6). In 2017, Li, H and coworker suggested that carboxylated multiwalled carbon nanotubes (c-MWCNTs) increase migration of RAW264.7 cells by stimulating the IP3/PLC/CRAC channel signalling pathway [55]. As previous reports suggest, gelsolin and ADF/cofilin play complementary roles to control the recycling of actin cytoskeleton regulated by calcium and phosphoinositides [56].…”

Section: Cell Signalling Initiated Through Zno5 Mwcnt5 and Msn15mentioning

confidence: 98%

MSN, MWCNT and ZnO nanoparticle-induced CHO-K1 cell polarisation is linked to cytoskeleton ablation

et al. 2021

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Background The cellular response to nanoparticles (NPs) for the mechanical clue and biochemical changes are unexplored. Here, we provide the comprehensive analysis of the Chinese Hamster Ovary (CHO-K1) cell line to study cell behaviour following the exposure of mesoporous silica nanoparticle (MSN), multiwall carbon nanotubes (MWCNTs), and zinc oxide (ZnO) NPs. Results Through the high-throughput proteomic study, we observed that the effect of NPs is alone not restricted to cell viability but also on cell polarisation. In the case of MSN, no drastic changes were observed in cellular morphology, but it upregulated chaperons that might prevent protein aggregation. However, MWCNT showed elongated cell appearance with numerous cytoplasmic vacuoles, and induce lamellipodia formation through actin polymerisation. The cytoskeleton remodelling was accompanied by the increased expression of Dlc-1, cofilin and Rac1 proteins. While ZnO NPs resulted in the rounded cell morphology along with nuclear abnormalities. The proteome analysis revealed that UBXN11 control cell roundness and DOCK3 leads to actin stress fibre formation and finally, loss of cell adhesion. It enhances the expression of catastrophic DNA damage and apoptotic proteins, which was unrecoverable even after 72 h, as confirmed by the colony formation assay. All three NPs trigger over-expression of the endocytic pathway, ubiquitination, and proteasomal complex proteins. The data indicate that ZnO and MSN entered into the cells through clathrin-mediated pathways; whereas, MWCNT invades through ER-mediated phagocytosis. Conclusions Based on the incubation and concentration of NPs, our work provides evidence for the activation of Rac-Rho signalling pathway to alter cytoskeleton dynamics. Our results assist as a sensitive early molecular readout for nanosafety assessment.

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Multi-walled carbon nanotubes act as a chemokine and recruit macrophages by activating the PLC/IP3/CRAC channel signaling pathway

Cited by 14 publications

References 47 publications

<p>The acute toxic effects of platinum nanoparticles on ion channels, transmembrane potentials of cardiomyocytes in vitro and heart rhythm in vivo in mice</p>

<p>The acute toxic effects of platinum nanoparticles on ion channels, transmembrane potentials of cardiomyocytes in vitro and heart rhythm in vivo in mice</p>

Resolution of Pulmonary Inflammation Induced by Carbon Nanotubes and Fullerenes in Mice: Role of Macrophage Polarization

MSN, MWCNT and ZnO nanoparticle-induced CHO-K1 cell polarisation is linked to cytoskeleton ablation

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