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Extracellular Vesicles (EVs)
Published in Peixuan Guo, Kirill A. Afonin, RNA Nanotechnology and Therapeutics, 2022
Alice Braga, Giulia Manferrari, Jayden A. Smith, Stefano Pluchino
Intercellular signaling is a finely regulated process fundamental to sustaining homeostasis and proper functioning of multicellular organisms. Cell-to-cell communication occurs through a diversity of chemical messengers, including small molecules, proteins, glycoproteins, lipids, growth factors, and even nucleic acids. These signaling molecules can act on the source cell via autocrine signaling, or adjacent cells via juxtracrine signaling, targeting neighbors direct contact via the formation of cell junctions (e.g. gap junctions). Soluble messengers like hormones, cytokines, and chemokines can also be released to act over longer distances through paracrine and endocrine signaling. In recent times, relatively long-distance (> 100 μm) cell-to-cell connections via membrane nanotubes have been described as another putative means of intercellular signaling for the exchange of genetic information or transfer of pathogens between distal cells (Davis and Sowinski 2008). Interestingly, these nanotubules seem to impede small molecules trafficking, facilitating instead the transfer of vesicle-packaged material (Rustom et al. 2004). Signaling vesicle secretion has been described in a multitude of different cell types, yet only a few specialized cases of short-range cell-to-cell communication mediated by EVs (e.g. synaptic exchanges between neurons (Sudhof 2004)) were formally recognized as canonical.
Introduction
Published in James E. Ferrell, Systems Biology of Cell Signaling, 2021
All living cells continually detect and respond to external signals. This is true for prokaryotes, whether they are living alone or in biofilms, and it is even more manifestly true in multicellular eukaryotes, where communication between cells and coordination of the cells’ behavior enables the organism to function as a unified whole. In large multicellular organisms like us humans, cells receive signals from their immediate neighbors through short-range signals like neurotransmitters and cell-surface molecules. They receive signals from more distant neighbors via longer range diffusible molecules such as morphogens and from still-more distant neighbors by means of hormones that flow through the circulatory system. They receive signals from the outside world via sense organs. Cells also monitor their own internal status, and there is a great deal of overlap between the cellular components involved in cell–cell communication and internal monitoring. Ultimately a cell processes input signals through a process termed signal transduction, shown schematically in Figure 1.1.
Single-Cell Analysis in Cancer
Published in Inna Kuperstein, Emmanuel Barillot, Computational Systems Biology Approaches in Cancer Research, 2019
Inna Kuperstein, Emmanuel Barillot
Multicellular organisms consist of different cell types that give rise to a multitude of organs and tissues with distinct functions. These cell type-specific functions are acquired during development in a process called cellular differentiation, whereby pluripotent stem cells undergo a sequence of gene expression changes to give rise to all mature cell types. Moreover, in adult organisms tissue-resident stem cells remain crucial for tissue homeostasis in organs with high turnover such as skin, gut or blood, where mature cell types constantly need to be replenished within a few days to maintain organ function.3 Yet in other organs, such as the liver, stem cells show lower turnover at homeostatic conditions, but can boost their proliferation significantly to regenerate tissue after injury.4
New binuclear dithiocarbamate complexes [M2-µ2-bis-{(κ2S,S-S2CN(R)CH2CONHC6H4)2CH2}] (M=NiII, CuII, and ZnII): synthesis, characterization, DFT, and in vitro cytotoxic study
Published in Journal of Coordination Chemistry, 2018
Vinay K. Singh, Vineeta Pillai, Prakash Gohil, Shailykumari K. Patel, Lipi Buch
Apoptosis is a genetically regulated programmed cell death that controls the development of multicellular organisms by maintaining cell populations in tissues, regulating immune system and aging. Basic oncology research highly focuses on genes and signals regulating apoptosis. The efficacy of cytotoxic drugs is measured by their ability to selectively promote apoptosis in cancer cells while causing less or no damage to normal healthy cells [7, 8, 61]. The shrinking of cells, a characteristic apoptotic sign [62], indicating the induction of apoptosis as part of the mechanism of action of these compounds can be clearly visualized by acridine orange/ethidium bromide (AO/EB) staining (Figure 7) which marks nuclear changes and differentiates between viable, apoptotic, and necrotic cells. Compounds viz. L’, L1, 1b, 1c, L2, L3, and 3a exhibiting lower IC50 values than cisplatin were stained for AO/EB wherein viable cells are stained by AO and show green fluorescence, whereas apoptotic cells are stained by EB and show orange to red fluorescence with condensed chromatin [63]. Contrary to our earlier results [38], we did not find DNA fragmentation for the abovementioned compounds, while the same showed clear cytotoxicity in AO/EB staining. The induction of apoptosis is further supported by morphological investigations carried out by using microscopic photographs of HepG2 upon 24 h exposure to the potent compounds and standard cisplatin at their respective in vitro IC50 values (Figure 8). The microscopic photographs clearly differentiate the normal proliferation of cells without any insult (control) from fewer proliferations of cells upon exposure of compounds such as L’, L1-L3, 1b, 1c, and 3a. These observations thus need further investigation to elucidate the exact mechanism and pathway of apoptosis being followed.
Lung tissue inflammatory response and pneumonocyte apoptosis of Sprague-Dawley rats after a 30-day exposure in methyl mercaptan vapor
Published in Journal of the Air & Waste Management Association, 2021
Lu Jiang, Jingjing Fang, Kexian Li, Xinhong Xu, Jiangbo Qiao
TUNEL-assays were consistent with result of inflammatory response of lung tissue, suggesting that apoptosis seemed to be triggered in a multifactorial way. Apoptosis is a fundamental biological process used to eliminate unwanted cells in a multicellular organism. In contrast to necrosis, which is a form of traumatic cell death that results from acute cellular injury, apoptosis is a highly regulated and controlled process that confers advantages during an organism’s lifecycle (Böhm and Schild 2003). Unlike necrosis, apoptosis produces cell fragments called apoptotic bodies that phagocytic cells are able to engulf and quickly remove before the contents of the cell can spill out onto surrounding cells and cause damage to the neighboring cells. Activation of apoptotic is an early important pathophysiological event in the development of indirect acute lung injury after hemorrhagic shock and sepsis, in which lung epithelial cells appear to play a central role. Twelve hours after acute lung injury, lung monocyte chemoattractant protein-1, keratinocyte-derived chemokine, macrophage inflammatory protein-2, IL-6, and TNF-α were increased (Perl et al. 2007). TNF is a cytokine produced mainly by activated macrophages, and is the major extrinsic mediator of apoptosis (Wajant 2002). TNF-α can also induce the activation of lung endothelial cells, migration of leukocytes, and granule cell degranulation and capillary leakage, and can increase rapidly systemic inflammatory response syndrome (Rossi, Pedone, and Antonelli 2011). It was reported that fibrotic lung disease occurs in the lungs of patients with idiopathic pulmonary fibrosis because of an abnormally activated, transforming growth factor-driven “aberrant repair process,” rather than inflammation (Krein and Winston 2002). An aberrant repair process may be a component of pulmonary fibrosis in scleroderma patients as well, with increased expression of intracellular transforming growth factor-β1 by bronchial epithelium and hyperplastic type II pneumonocytes (Corrin et al. 1994). In the early stage of lung inflammation, alveolar macrophages’ release of cytokines such as TNF-α, interferon gamma activated macrophages (interferon gamma, IFN-r), and prostaglandin E2 (prostaglandinE2, PGE2) can induce inflammatory reaction (Rettew, Huet, and Marriott 2009).