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Nanotoxicology and Regulatory Aspects of Nanomaterials and Nanomedicines
Published in Yasser Shahzad, Syed A.A. Rizvi, Abid Mehmood Yousaf, Talib Hussain, Drug Delivery Using Nanomaterials, 2022
Clathrin-dependent endocytosis is the most characterized endocytosis process as far it's the most active and constitutively present in all types of cells (Wang et al., 2020). Its role is essential for the cellular hemostasis for nutrients and macromolecule transport such as cholesterol via low density lipoproteins (LDL receptors), and iron via transferrin (Tfn receptors) that are considered as markers for this route of uptake, serum proteins, membranous ion pumps. It has a crucial role in cellular communication during organogenesis, cell signalling regulation by controlling and downregulation of receptor levels, synaptic neuronal transmission (Ca+2-gated channels regulation, recycling of neurotransmitter vesicles), and reabsorption of serum proteins after filtration in kidney tubules (Kaksonen and Roux, 2018; López-Hernández et al., 2020). It is membranous invaginations mediated through clathrin triskelia that coat or cage the incoming vesicles (Conner and Schmid, 2003). It is initiated by a binding of certain ligands to surface receptors at clathrin-nucleation sites/pits with subsequent clathrin-1 protein assembly with the adaptor/assembly protein complexes into clathrin-coated lattices. Dynamin GTPase scission mechanism proceeds around the vesicle neck. Clathrisome disassemble its coatings prior to fusion with the endolysosmes. The molecules/particles size ranges from ~100 to 200 nm (Wang et al., 2020).
Cell Penetrating Peptide (CPP)–Modified Liposomal Nanocarriers for Intracellular Drug and Gene Delivery
Published in Mansoor M. Amiji, Nanotechnology for Cancer Therapy, 2006
Two types of the endocytic uptake of the CPPs have been proposed: the classical clathrin-mediated endocytosis and the lipid-raft-mediated caveolae endocytosis. Clathrin-mediated endocytosis involves the formation of clathrin-coated membrane pits that pinch off the membrane to form vesicles for subsequent processing.52 This type of endocytosis was suggested in Console et al. where the TAT peptide showed the co-localization with the classical endocytic marker, transferrin. This was substantiated further in Lundberg, Wilkstrom, and Johansson where TAT PTD and Antp PTD showed uptake only at 37°C. In addition, the internalization required the expression of negatively charged glycosaminoglycans on the cell surface for interaction with CPPs that was followed by endocytosis. Studies also suggested that the PTDs do not provoke a real translocation, but they are only responsible for cell surface adherence that subsequently results in their endocytosis and accumulation in endosomes.53–57 In fact, direct electrostatic interaction between the positive residues of CPPs and the negative residues of the cell-surface proteoglycans or glycosaminoglycans (such as heparan sulfate, heparin) is required in internalization regardless of the mechanism of cellular uptake54,58–60 although some studies suggested the lack of correlation between proteoglycans and transduction process.61
Antiviral Nanomaterials as Potential Targets for Malaria Prevention and Treatment
Published in Devarajan Thangadurai, Saher Islam, Charles Oluwaseun Adetunji, Viral and Antiviral Nanomaterials, 2022
Kantrol Kumar Sahu, Sunita Minz, Madhulika Pradhan, Monika Kaurav, Krishna Yadav
Pinocytosis is classified as caveolae-mediated endocytosis, clathrin-mediated endocytosis clathrin- and caveolae-independent endocytosis, and micropinocytosis (Sun et al. 2019) (Table 18.2). Caveolar-mediated endocytosis is a clathrin-independent endocytotic mechanism involving bulb-shaped caveolae. Caveolae are 50-60 nm plasma membrane invaginations. Caveolae are formed by caveolins, which are integral membrane proteins, and cavins are peripheral membrane proteins. Clathrin-mediated endocytosis possesses complex protein machinery that transiently assembles on the plasma membrane and creates clathrin-coated endocytic vesicles. This machinery selects and concentrates cargo molecules and shapes the membrane into a vesicle.
Epidemiology, virology and clinical aspects of hantavirus infections: an overview
Published in International Journal of Environmental Health Research, 2022
Sima Singh, Arshid Numan, Dinesh Sharma, Rahul Shukla, Amit Alexander, Gaurav Kumar Jain, Farhan Jalees Ahmad, Prashant Kesharwani
Following attachment to a cell surface receptor, the Hantavirus virus is incorporated into the host population. After binding, cell entry is mediated through clathrin-coated pits, and virons are eventually delivered to lysosomes. Virions are uncoated inside the endolysosomal compartment, and three viral capsids are released into the cytoplasm (Jin et al. 2002). This causes the virus to be taken up by a clathrin-coated vesicle (CCV), which is made up of clathrin-coated cellular membrane (Ramanathan and Jonsson 2008). RdRp initiates transcription and produces three mRNAs, one from each S, M, and L section of the viral RNA. The S and L derived mRNAs are translated on free ribosomes. Although M-specific mRNAs are translated on the rough endoplasmic reticulum (ER). Intrinsically, the glycoprotein precursor is cleaved at a closely conserved amino acid motif, yielding two glycoproteins, Gn and Gc (Spiropoulou 2000). The glycoproteins Gn and Gc are transferred to the Golgi complex for glycosylation. Following glycosylation in the ER, Gn and Gc transfer to the Golgi complex. Hanta virions are assumed to form in the Golgi complex. It is accompanied by budding into the Golgi cisternae, migration to the plasma membrane of secretory vesicles, and exocytosis. However, the specifics of virion egress mostly remain unknown (Szabó 2017).
Environmental transformation and nano-toxicity of engineered nano-particles (ENPs) in aquatic and terrestrial organisms
Published in Critical Reviews in Environmental Science and Technology, 2020
Qumber Abbas, Balal Yousaf, Habib Ullah, Muhammad Ubaid Ali, Yong Sik Ok, Jörg Rinklebe
The cellular uptake mechanisms of ENPs across plasma membrane involved passive transport (diffusion or perisorption), endocytosis and non-endocytosis pathways. Diffusion is the dominant trafficking process across membranes for small (<5 nm), positively charged and hydrophobic ENPs (Baker et al., 2014). The cellular uptake pathway and mechanism of nano toxicity in multicellular organisms is shown in Figure 4. Perisorption of smaller, positively charged particles may occur through intestine microvilli/villi, enterocyte cells in paracellular-tight junction channels and enterocyte protrusion gaps (Cornelis et al., 2014). Primarily intact ENPs enter the tissues through endocytosis pathway and respiratory or digestive systems epithelial tissue lines are the potential sites for this uptake process. Receptor-mediated endocytosis (RME), also known as clathrin-mediated endocytosis directed the ENPs toward the organism lysosome. This endocytosis pathway may cause the intracellular toxicity due to the high content of labile metal ions through a process called “Trojan horse” effect. Other endocytosis pathways including caveolae/lipid raft-dependent endocytosis and macropinocytosis did not transport the ENPs for lysosomal degradation, but inside cell, particles remain in nano-form (Tangaa et al., 2016). Ions released as a result of ENPs dissolution are internalized in the cell through transporter proteins or ion channels. For instance, Na ion channels are involved in the uptake of ionic Ag in freshwater fish rainbow trout (Bury & Wood, 1999).