纳米粒子与细胞相互作用的力学–化学偶联研究进展

doi:10.3866/PKU.WHXB201905076

Abstract

Abstract:

The biosafety of nanoparticles is gaining extensive attention due to their dichotomous effects in fields of biomedicine and atmospheric chemistry. A number of studies have been carried out focusing on the cytotoxicity of nanoparticles and their interactions with cells. However, the mechanism of nanoparticle–cell interactions remains unclear. Here, we review the latest progress in the study of nanoparticle-cell interactions from a cellular chemo-mechanical perspective. Cell mechanics play an important role in cell differentiation, proliferation, apoptosis, polarization, adhesion, and migration. An understanding of the effects of nanoparticles on cell mechanics is therefore needed in order to enhance comprehension of nanoparticle–cell interactions. Firstly, the main molecules and signal pathways related to mechanical chemistry are introduced from three perspectives: cell surface adhesion receptors, the cytoskeleton, and the nucleus. Specifically, integrins and cadherins play a critical role in sensing both the external mechanical force and the force of cell transmission. Actin and microtubules, which are two components of the cytoskeletal network, act as a bridge in mechanical conduction. The nucleus can also be mechanically stressed by the surrounding cytoskeleton through the contraction of the matrix. The nuclear envelope also plays important roles in sensing mechanical signals and in adjusting the morphology and function of the nucleus. We summarize the major nanoparticle-based tools used in the laboratory for the study of cell mechanics, which includes traction force microscopy, atomic force microscopy, optical tweezers, magnetic manipulation, micropillars, and force-induced remnant magnetization spectroscopy. In addition, we discuss the effects that nanoparticles have on cell mechanics. Nanoparticles interact with the adhesion of molecules on the cell membrane surface and on cell cytoskeletal proteins, which further affects the mechanical properties involved in cell stiffness, cell adhesion, and cell migration. Overall, the general conclusions regarding the effects of nanoparticles on cell mechanics are as follows: (1) Nanoparticles can affect cell adhesion by disrupting tight and adherent junctions, and by regulating cell-extracellular matrix adhesion; (2) Nanoparticles can interact with cytoskeletal proteins (actins and tubulins) leading to structural reorganization or disruption of microtubules and F-actin; (3) Cell stiffness changes with the structural reorganization of the cytoskeleton; (4) Cell migration ability can be affected through changes in the cytoskeleton, cell adhesion, and the expression of cell migration-related proteins/molecules. To develop the nano-biosafety evaluation system, future studies should attempt to gain a better understanding of the molecular mechanisms involved with regards to nanoparticles and cell mechanics. Ultimately, further development of new methods and technologies based on nano-mechanical chemistry for diagnosis and treatment purposes are expected, given the wide application of nanomaterials in the biomedical field.

Key words: Nanoparticle, Cell, Mechanotransduction, Interaction, Mechanochemical coupling

Jinxiu Zhan,Feng Feng,Min Xu,Li Yao,Maofa Ge. Progress in Chemo–Mechanical Interactions between Nanoparticles and Cells[J]. Acta Physico-Chimica Sinica 2020, 36(1), 1905076. doi: 10.3866/PKU.WHXB201905076

Figures/Tables 4

Fig 1

Fig 2

Fig 3

Table 1

Effects of nanoparticles on cell mechanics."

Particle type	Size and zeta potential	Cell types	Incubation conditions	Impacts on cell mechanics	Ref.
Iron-iron oxide	16 ± 1.5 nm	BAC	5, 10, 20, 50 μg·mL^?1;	Increase in Young’s modulus of BACs with	55
core-shell MNPs			3 days	the increase of NP concentration.
Ag NPs	20 nm	USC	0–64 μg·mL^?1;	Increase in actin polymerization and	53
			5 × 10³ cells·well^?1; 24 h	cytoskeletal tension, activation of RhoA
Nano-Si64 and	63.88 ± 10.35,	L-02	10, 20, 50 μg·mL^?1;	Change in quantity and distribution of	50
Nano-Si46	46.15 ± 5.53 nm;		1×10⁵ cells·mL^?1;	cytoskeleton through extra ROS and Ca²⁺
	negatively charged		24 h	leading to abnormal mitosis and cytokinesis
AgNPs	52.3 ± 8.7 nm (single NP);	MG-63	0.5, 5, 10, 20 μg·mL^?1;	Destruction of F-actin in quantity and	51
	201 nm (aggregates);		2 × 10⁴ cells·well^?1;	structure, decrease in expressions of ALP,
			24, 48, 72 h	OCN and COL-I in a dose-dependent manner
TiO₂-PEG NPs	100, 200, 300 nm	NCI-H292	100 μg·mL^?1;	NP-mediated promotion of the lysosomal	58
			8 × 10⁴ cells?cm^?²;	degradation of integrin beta 1, thus leading to
			3 h	reduced expression of pFAK and cytoskeletal
				reduced expression of pFAK and cytoskeletal
Fullerenol NPs	1.72 ± 0.14 nm	MCF-7,	200 μg·mL^?1;	Lowered stiffness and restrained migration,	47
		MDA-MB-231	5 × 10⁵ cells·well^?1;	decrease in the number and length of
			24 h;	filopodia, change in cancer cell adhesion and
				motility through the inhibition of integrin to
				form clusters on filopodias
GO Nanosheets	2 nm (thickness);	A549	50 μg·mL^?1;	Retardation of cell migration through	57
	397.6 ± 62.4 nm;		6 h, 24 h	nanosheet-mediated disruption of intracellular
	?34.8 ± 1.0 mV			actin filaments.
Ag NPs and	10 nm	CCD-1072Sk	0.1, 1, 10 μg·mL^?1;	Reduce in collagen and laminin production	59
Au NPs			5×10³/8-well;	and cell migration, increase in the formation
			24 h	of stress fibers and the number of cell
				protrusions, impaired cell polarity.
SPIONs	132.4 nm; ?25.37 mV	VFF	20, 40, 80 μg·cm^?2; 24 h	Decrease in VFF adhesion	49
Si NPs and	7 nm	MSC	100 μg·mL^?1’;	Structural reorganization of cortical	56
SiB NPs			3 × 10³ cells?cm^?²;	cytoskeleton with subsequent stiffness
			1 and 24 h	increase and concomitant F-actin content
TiO₂	15–50 nm (single NP);	TR146	125, 1250 μmol?L^?1;	Increase of long vinculin near the cell–cell	5
SiO₂	272 ± 4, 236 ± 25 236 ± 9		90 000 cells?cm^?²;	boundary and traction force, low level of MT
HA	nm (aggregates); negatively		12 h	acetylation, maturation of FAs, destabilization
	charged			of MT networks, promotion of cell adhesion
				and retardation in cell migration
TiO₂ NPs	18–23 nm;≈?20 mV	MCF-7, MDA-MB-231,	0–40 μg·mL^?1;	Destruction of adherence junctions which	48
SiO₂ NPs		SW620	0.5 and 24 h	induced endothelial leakiness and promoted
Au NPs				the metastasis of breast cancer cells
Magnetoliposomes	14.0，4.2–4.8，4.2	NPCs and	500, 1000 μg·mL^?1;	Reduce in cellular proliferation, expression of	52
Endorem	and 4.0 nm	hBOECs	5×10⁴ cells·well^?1;	FAK and distribution of actin cytoskeleton
Resovist			24 h	and microtubule network
very small organic
particles

Table 1

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