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Lysosomal Ion Channels and Human Diseases
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Peng Huang, Mengnan Xu, Yi Wu, Xian-Ping Dong
TPCs play an important role in endolysosomal membrane trafficking. Castonguay et al. suggest that TPC1 channel interacts with syntaxins to regulate the fusion of intracellular vesicles, and TPC1 deficiency impairs efficient protein processing through early and recycling endosomes (Castonguay et al., 2017). Grimm et al. (2014) suggest that cells lacking TPC2 display a profound impairment of low-density lipoprotein (LDL)-cholesterol and epithelial growth factor (EGF)/EGF-receptor trafficking, likely due to a defective fusion between the late endosome and the lysosome. It is also suggested that TPC2 ablation disturbs integrin trafficking in the endolysosomal system (Nguyen et al., 2017). In contrast to LDL-cholesterol and EGF/EGF-receptors that are accumulated in late endosomes, integrins are enriched in early endosomes. TPC2 deletion also causes impaired membrane trafficking of melanosomes, lysosome-related organelles (Ambrosio et al., 2016).
Atomic Force Microscopy of Biomembranes
Published in Qiu-Xing Jiang, New Techniques for Studying Biomembranes, 2020
Yi Ruan, Lorena Redondo-Morata, Simon Scheuring
During membrane trafficking, a myriad of proteins act in concert to promote the formation of membrane carriers through membrane remodeling. Previous studies have shown that membrane remodeling proteins perform their functions through several modes. ESCRT-III (Endosomal Sorting Complex Required for Transport) has been implicated in the formation of Intralumenal Vesicles (ILVs) during biogenesis of Multi-Vesicular Bodies (MVBs) by genetic69 and biochemical assays.70,71 This budding process has a topology opposite to the membrane invaginations occurring during endocytosis and membrane traffic at the endoplasmic reticulum or Golgi. In MVBs, the limiting membrane is pushed outwards from the cytoplasm instead of curving inwards. ESCRT-III has been proposed to play a role in membrane deformation72 and fission of ILVs.70 However, it is unclear how ESCRT-III deforms lipid membranes. Because of their polymerization abilities, ESCRT-III proteins (Vps20, Snf7, Vps2, Vps24) have been proposed to generate membrane curvature by scaffolding.73,74
Identifying Nanotoxicity at the Cellular Level Using Electron Microscopy
Published in Suresh C. Pillai, Yvonne Lang, Toxicity of Nanomaterials, 2019
Kerry Thompson, Alanna Stanley, Emma McDermott, Alexander Black, Peter Dockery
Endocytosis is generally a more complicated process in polarised in vitro epithelial cell systems in comparison to the non-polarised phenotype. This is due to the ability of the polarised cell to carry out internalisation of macromolecules from both the apical and basolateral surfaces (Apodaca, 2001). The actin microfilament and microtubule cytoskeletal components are thought to play pivotal roles in the endocytic process (Di Fiore and Scita, 2003, Kornilova, 2014). Not only do these filamentous structures provide the tracks along which endocytosed vesicles are shuttled, but the GTPase sub-families which control them, Rho and Rab, are thought to provide integrated control of both membrane trafficking and cytoskeletal reorganisation (Feng et al., 1995, Di Fiore and Scita, 2003).
Effects of caffeic acid phenethyl ester use and inhibition of p42/44 MAP kinase signal pathway on caveolin 1 gene expression and antioxidant system in chronic renal failure model of rats
Published in Drug and Chemical Toxicology, 2023
Yilmaz Cigremis, Hasan Ozen, Merve Durhan, Selahattin Tunc, Evren Kose
Caveolae are 50–80 nm diameter sack-like invaginations of the plasma membrane that are present in many cell types (Lamaze et al. 2017). They are highly important in membrane trafficking and play important roles in cellular bioactivities. Caveolae are composed of caveolins (CAV) and cavins. Three types of caveolins, CAV1, CAV2, and CAV3 are described. CAV1 is expressed in many cell types, such as adipocytes, endothelial cells, pneumocytes, fibroblasts, and smooth muscle cells (Cohen 2004). It is also shown to be normally expressed in distal convoluted tubules, collecting ducts, and parietal cells of Bowman capsule of normal human kidney (Tamaskar et al. 2007). Although CAV1−/− knockout mice were reported to be viable and fertile, lack of caveolae or caveolins were shown to cause muscle, pulmonary, or lipid disorders (Le Lay and Kurzchalia 2005). A wide distribution of CAV1, therefore, signifies its importance in cellular transmembrane activities.
Canalicular system reorganization during mouse platelet activation as revealed by 3D ultrastructural analysis
Published in Platelets, 2021
Irina D. Pokrovskaya, Michael Tobin, Rohan Desai, Smita Joshi, Jeffrey A. Kamykowski, Guofeng Zhang, Maria A. Aronova, Sidney W. Whiteheart, Richard D. Leapman, Brian Storrie
The discovery of the platelet canalicular system (CS), an open network of randomly distributed, often interconnected, membrane-limited, tubular channels, dates to the late 1960s [1,2]. This discovery was attributed then to “improved” methods for electron microscopy sample preparation [3]. Based on its morphology, CS has drawn attention as a possible pathway for the uptake of external substances to platelet organelles [4], as a putative conduit for the extrusion of α-granule stored proteins [3–6], and as a membrane reservoir for expansion of platelet surface area during platelet activation/spreading [7]. A fourth, possible general role as a structural intermediate in membrane trafficking processes, e.g., endocytosis, phagocytosis, and exocytosis has been questioned [8–12]. The proposed roles of the CS as a structural conduit to and from the platelet interior and as a membrane reservoir could well be logically considered to be time-shared between resting and activated platelet states. In brief, the CS’s properties, and by extension its proposed function, appear varied and the subject of some controversy [13]
Small GTPases in platelet membrane trafficking
Published in Platelets, 2019
Tony G. Walsh, Yong Li, Andreas Wersäll, Alastair W. Poole
Membrane trafficking describes a form of cellular communication involving the movement of cargo (e.g. proteins, lipids or pathogens), within membrane bound vesicles, towards spatially distinct compartments. This is a multistep process involving initial vesicle formation from a donor organelle membrane where cargo is packaged (e.g. trans-Golgi network), movement of this ‘carrier’ vesicle towards an acceptor organelle (e.g. early endosome) and, tether to an acceptor with subsequent membrane fusion allowing release of carrier cargo into the lumen of the target organelle [1]. Classically, two of the principal roles for membrane trafficking are exocytosis and endocytosis, which terminate or initiate at the plasma membrane, respectively. At the heart of these processes is the biosynthetic pathway primarily composed of the endoplasmic reticulum (ER) and Golgi complexes to orchestrate the sorting of correctly folded proteins into vesicles, prior to trafficking to a target organelle. These complex and tightly regulated processes are fundamental to eukaryotic cell function, and as such, the Nobel Prize in Physiology or Medicine 2013 was awarded to three pioneering scientists (Rothman, Schekman & Sϋdhof) who discovered key molecular regulators of vesicular traffic in mammalian cells [2].