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Fig. 6 | Journal of Nanobiotechnology

Fig. 6

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

Fig. 6

Schematic representation of the distinct pathway for internalisation of MSN, MWCNT, and ZnO NPs in CHO-K1 cells: The proposed mechanism involved MSN and ZnO NPs uptake through clathrin-mediated endocytosis. Phase 1, NPs binds with clathrin and adaptor proteins to form a clathrin-coated pit. The clathrin uncoated vesicles fused with early endosomes for subsequent endolysosomal trafficking. MWCNT internalised via ER-meditated phagocytosis involve the assembly of coronin, F-actin and other adaptor proteins on the plasma membrane for subsequent intracellular trafficking. ER play an essential role for recycling the receptor. Two distinct pathway regulate Rac1 pathway to modulate cytoskeleton dynamics or cell morphology. MWCNT synergise with other cell surface receptors like Cav to activate Ca2+ signaling through the ER. Ca2+ signaling linked to Rac1 pathway through DOCK3 protein. On the other hand, receptor tyrosine kinase (RTK) involved in Rho-Rac mediated signaling pathway to regulate the F-actin polymerisation. ZnO NPs upregulate the UBXN11 that induced the actin stress fiber formation and causes the cell rounding. The internalisation of ZnO nanoparticle can activate P53 signaling pathways and subsequently affect DNA damage repair mechanism and cell cycle arrest

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