Search

The evolution of next-generation neural interfaces toward high-density, high-fidelity, and long-term recordings coupled with the advent of complex fabrication techniques drives the development of 3D nanostructures to bridge the neuron-artificial device interface. This is largely due to several observations of high signal-to-noise ratios recorded from high-aspect-ratio 3D nanoelectrodes enabled by an inimitable mechanical coupling with the neural membrane and, in some cases, direct access to the neural intracellular space. This review details progress in developing 3D electrodes for electrogenic cell interfaces. First, the impacts of nanotopography on the electrical and mechanical coupling of the cell and recording electrodes are discussed, and different conceptual approaches in understanding the biomechanics of cell/3D electrode coupling through experimental work and computational models are described. This work also highlights the latest advances in 3D nanostructures for recording the intracellular activity of cultured neurons and cardiomyocytes with a focus on emerging 3D structures and strategies aimed at improving efficiency and long-term integration with cultured electrogenic cells.

Summary: Macrophages must not only be responsive to an array of different stimuli, such as infection and cellular damage, but also perform phagocytosis within the diverse and complex tissue environments found in vivo. This requires a high degree of morphological and therefore cytoskeletal plasticity. Here, we use the exceptional genetics and in vivo imaging of Drosophila embryos to study macrophage phagocytic versatility during apoptotic corpse clearance. We find that macrophage phagocytosis is highly robust, arising from their possession of two distinct modes of engulfment that utilize exclusive suites of actin-regulatory proteins. “Lamellipodial phagocytosis” is Arp2/3-complex-dependent and allows cells to migrate toward and envelop apoptotic corpses. Alternatively, Diaphanous and Ena drive filopodial phagocytosis to reach out and draw in debris. Macrophages switch to “filopodial phagocytosis” to overcome spatial constraint, providing the robust plasticity necessary to ensure that whatever obstacle they encounter in vivo, they fulfil their critical clearance function.

This paper treats the phenomenon of phagocytosis from the flow of energy point of view. Considerable efforts have been made towards elucidating the subject of phagocytosis in other fields of learning, but little has been said about the mechanical work that is done during phagocytosis. Phagocytosis without doubt is an interaction that involves the flow of energy. Energy equation model of phagocytosis is then presented in this paper to analyze the mechanical energy that is involved in the build-up of the engulfment of bacteria by the phagocytes. Data of the E Coli bacteria from published work was then applied to the solution of the energy equation. A borderline contact angle ϑ of 77.356° between the phagocyte and the bacteria at χ=0 was deduced in this work. It was shown that when ϑ77.356°, χ>0, engulfment is not favoured for E-coli. This condition is conceptually in line with ΔFNET approach reported in the literature. Data of four different bacterial species were also used to plot the graphs of the engulfment parameter χ against contact angle ϑ which revealed that the more hydrophobic bacteria are easily phagocytized than the more hydrophilic ones.

Phospholipids are asymmetrically distributed at the plasma membrane. Phosphatidylserine (PtdSer) is exclusively located in the inner leaflet of the cell membrane while phosphatidylcholine (PtdCho) and glycolipids are mainly located in the outer leaflet of the membrane. However, this asymmetry is disrupted in various physiological situations, and PtdSer is exposed on the cell surface. In platelets, exposed PtdSer functions as a scaffold for the coagulation reaction, while in dead cells, exposed PtdSer serves as an "Eat-me" signal for efferocytosis. In the developing brain, synaptic connections are over-formed during the fetal period, but about half of the neurons are removed by apoptosis, and synaptic and dendritic compartments of living neurons are also removed by phagocytes. During these processes, glial cells such as microglia and astrocyte engulf unwanted dead cells and compartments in living cells using several phagocytic receptors, recognizing PtdSer by direct binding or an indirect way using secreted molecules. Based on recent findings, we will discuss how the compartments in living neurons are eliminated for the neuronal circuit plasticity., (Copyright © 2021. Published by Elsevier B.V.)

Phagocytosis is an essential process by which cellular debris and pathogens are cleared from the environment. Cells extend their plasma membrane to engulf objects and contain them within a limiting membrane for isolation from the cytosol or for intracellular degradation in phagolysosomes. The basic mechanisms of phagocytosis and intracellular clearance are well conserved between animals. Indeed, much of our understanding is derived from studies on the nematode worm, Caenorhabditis elegans. Here, we review the latest progress in understanding the mechanisms and functions of phagocytic clearance from C. elegans studies. In particular, we highlight new insights into phagocytic signaling pathways, phagosome formation and phagolysosome resolution, as well as the challenges in studying these cyclic processes., (Copyright © 2021 Elsevier Inc. All rights reserved.)

RNA-binding proteins (RBPs) are essential regulators of gene expression that act through a variety of mechanisms to ensure the proper post-transcriptional regulation of their target RNAs. RBPs in multiple species have been identified as playing crucial roles during development and as having important functions in various adult organ systems, including the heart, nervous, muscle, and reproductive systems. ETR-1, a highly conserved ELAV-Type RNA-binding protein belonging to the CELF/Bruno protein family, has been previously reported to be involved in C. elegans muscle development. Animals depleted of ETR-1 have been previously characterized as arresting at the two-fold stage of embryogenesis. In this study, we show that ETR-1 is expressed in the hermaphrodite somatic gonad and germ line, and that reduction of ETR-1 via RNA interference (RNAi) results in reduced hermaphrodite fecundity. Detailed characterization of this fertility defect indicates that ETR-1 is required in both the somatic tissue and the germ line to ensure wild-type reproductive levels. Additionally, the ability of ETR-1 depletion to suppress the published WEE-1.3-depletion infertility phenotype is dependent on ETR-1 being reduced in the soma. Within the germline of etr-1(RNAi) hermaphrodite animals, we observe a decrease in average oocyte size and an increase in the number of germline apoptotic cell corpses as evident by an increased number of CED-1::GFP and acridine orange positive apoptotic germ cells. Transmission Electron Microscopy (TEM) studies confirm the significant increase in apoptotic cells in ETR-1-depleted animals, and reveal a failure of the somatic gonadal sheath cells to properly engulf dying germ cells in etr-1(RNAi) animals. Through investigation of an established engulfment pathway in C. elegans, we demonstrate that co-depletion of CED-1 and ETR-1 suppresses both the reduced fecundity and the increase in the number of apoptotic cell corpses observed in etr-1(RNAi) animals. Combined, this data identifies a novel role for ETR-1 in hermaphrodite gametogenesis and in the process of engulfment of germline apoptotic cell corpses., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Prey spectrum and feeding process of the mixotrophic thecate dinoflagellate Fragilidium mexicanum strain Fm-LOHABE01 were examined using a culture isolated from Masan Bay, Korea in 2011 during a summer bloom of the toxic dinoflagellate Alexandrium pacificum. The novel 18S and 28S rDNA sequences for F. mexicanum were also used to explore inter-species relationships within the genus Fragilidium. The F. mexicanum fed on species belonging to four dinoflagellate genera (i.e., Alexandrium, Ceratium, Heterocapsa, and Scrippsiella) when separately offered a variety of prey, including dinoflagellates, raphidophytes, cryptophytes, and a ciliate. In addition, F. mexicanum displayed different levels of feeding frequency for prey species of Alexandrium. While F. mexicanum consistently fed on A. catenella and A. pacificum, feeding on A. affine was rarely observed. The F. mexicanum ingested prey by direct engulfment through the sulcus, after capturing the prey by a tow filament. Phylogenetic analyses of 18S and 28S rDNA datasets demonstrated that Fragilidium sequences formed a monophyletic group with high statistical supports and diverged into four distinct clades. The F. mexicanum formed a separate clade with Fragilidium sp. EUSK D from Angola and Korean isolate of F. fissile with very strong supports., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Programmed cell clearance is a highly regulated physiological process of elimination of dying cells that occurs rapidly and efficiently in healthy organisms. It thus ensures proper development as well as homeostasis. Recent studies have disclosed a considerable degree of conservation of cell clearance pathways between nematodes and higher organisms. The externalization of the anionic phospholipid phosphatidylserine (PS) has emerged as an important "eat-me" signal for phagocytes and its exposition on apoptotic cells is controlled by phospholipid translocases and scramblases. However, there is mounting evidence that PS exposure occurs not only in apoptosis, but may also be actively expressed on the surface of cells undergoing other forms of cell death including necrosis; PS is also expressed on the surface of engulfing cells. Additionally, PS may act as a "save-me" signal during axonal regeneration. Here we discuss mechanisms of PS exposure and its recognition by phagocytes as well as the consequences of PS signaling in nematodes and in mammals., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Apoptotic cells are engulfed and digested by macrophages to maintain homeostasis in animals. If dead cells are not engulfed swiftly, they undergo secondary necrosis and release intracellular components that activate the immune system. Apoptotic cells are efficiently cleared due to phosphatidylserine (PtdSer) exposed on the cell surface that acts as an "eat me" signal. PtdSer is exposed through the activation of phospholipid scramblase and the inactivation of phospholipid flippase, which are both caspase-mediated events. Macrophages express a variety of molecules to recognize PtdSer, and use a sophisticated mechanism to engulf apoptotic cells. In red blood cells, the nucleus is lost when it is extruded as a pyrenocyte during definitive erythropoiesis. These pyrenocytes (nuclei surrounded by plasma membrane) also expose PtdSer on their surface and are efficiently engulfed by macrophages in a PtdSer-dependent manner. Macrophages transfer the engulfed apoptotic cell or pyrenocyte into lysosomes, where the components of the dead cell or pyrenocyte are degraded. If lysosomes cannot digest the DNA from apoptotic cells or pyrenocytes, the undigested DNA accumulates in the lysosome and activates macrophages to produce type I interferon (IFN) via a STING-dependent pathway; in embryos, this causes severe anemia. Here, we discuss how macrophages clear apoptotic cells and pyrenocytes., (© 2015 Elsevier Inc. All rights reserved.)

Programmed cell death occurs in the germline of many organisms, both as an essential part of development and throughout adult life. Germline cell death can be apoptotic or nonapoptotic, depending on the stimulus or stage of development. Here, we focus on the Drosophila ovary, which is a powerful model for studying diverse types of cell death. In Drosophila, the death of primordial germ cells occurs normally during embryonic development, and germline nurse cells are programmed to die during oocyte development in adult flies. Cell death of previtellogenic egg chambers in adults can also be induced by starvation or other environmental cues. Mid-oogenesis seems to be particularly sensitive to such cues and has been proposed to serve as a checkpoint to avoid the energetically expensive cost of egg production. After the germline dies in mid-oogenesis, the remnants are engulfed by an epithelial layer of follicle cells; thus, the fly ovary also serves as a highly tractable model for engulfment by epithelial cells. These examples of cell death in the fly ovary share many similarities to the types of cell death seen in the mammalian germline. Recent progress in elucidating the molecular mechanisms of cell death in the germline is discussed., (© 2015 Elsevier Inc. All rights reserved.)

The thymus provides the microenvironment in which thymocytes develop into mature T-cells, and interactions with thymic stromal cells are thought to provide the necessary signals for thymocyte maturation. Recognition of self-MHC by T-cells is a basic requirement for mature T-cell functions, and those thymocytes that do not recognize or respond too strongly to the peptide-loaded self-MHC molecules found in the thymus undergo apoptosis. As a result, 95% of the thymocytes produced will die and be subsequently cleared by macrophages. This review describes a complex crosstalk between developing thymocytes and engulfing macrophages which is mediated by retinoids produced by engulfing macrophages. The interaction results in the harmonization of the rate of cell death of dying double positive cells with their clearance and replacement, and in promotion of the differentiation of the selected cells in the thymus., (Copyright © 2013 Elsevier GmbH. All rights reserved.)