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Nanoengineering Neural Cells for Regenerative Medicine
Published in Klaus D. Sattler, st Century Nanoscience – A Handbook, 2020
Christopher F. Adams, Stuart I. Jenkins
In terms of its cytoarchitecture, the CNS consists of two major classes of cells: the neurons and their supporting glia. Neurons transmit electrical signals and reside in groups forming multiple connections with other neurons to make up neural circuits, which perform a common function, for example, vision or movement (Bear, Connors and Paradiso, 2015). Neurons extend axons which are highly specialized structures unique to neuronal cells and adapted to relay information within the body. Axons are ensheathed by layers of an electrically-insulating fatty deposit called myelin. CNS myelin is made and maintained by the oligodendrocytes, each of which can myelinate multiple axons. Astrocytes are the major supporting cell type within the CNS, with new roles regularly being discovered. Their currently accepted functions include: maintaining CNS homeostasis; clearance and recycling of neurotransmitters; providing metabolic support to neurons; roles in synapse formation and maintenance (Bear, Connors and Paradiso, 2015; Liddelow and Barres, 2015; Verkhratsky and Butt, 2013).
Mechanobiology in Health and Disease in the Central Nervous System
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
Theresa A. Ulrich, Sanjay Kumar
The mechanical properties of the ECM can direct a wide range of cellular properties, including cell shape and cytoarchitecture [33–35], motility [36,37], matrix remodeling [38], differentiation [39–42], and the extension of functional cellular projections [43–46]. As the human brain develops, billions of cells are generated in the proliferative tissues lining the lateral ventricles of the brain. These cells migrate throughout the developing CNS, differentiate into neurons or glial cells, and establish a diverse array of organized structures with distinctive shapes and intricate internal architecture [47]. Neurogenesis continues, albeit in a much more limited way, into adulthood through the self-renewal and differentiation of adult neural stem cells (aNSCs) found within the hippocampus and subventricular zone [48]. The mechanosensitivity of aNSCs was recently explored by Saha et al., who demonstrated that the differentiation and self-renewal of aNSCs can be modulated by controlling the mechanical stiffness of the surrounding microenvironment [42]. In particular, culturing aNSCs on the surface of soft polymeric substrates with stiffnesses close to living brain tissue (∼100–500 Pa) favored differentiation into neurons, whereas culturing aNSCs on polymeric substrates with identical surface chemistry but much greater mechanical rigidity (∼1–10 kPa) favored differentiation into glial cell types. The latter finding raises the intriguing possibility that tissue stiffening may play an instructive role in glial scar formation rather than merely serving as a passive consequence of the process. This mechanosensitivity, coupled with the mechanical heterogeneity present throughout the normal and diseased brain, lends support to the hypothesis that mechanical cues may be dynamically involved in CNS development, in the maintenance of homeostasis, and in the development of disease.
Renal damage induced by the pesticide methyl parathion in male Wistar rats
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Victor Hugo Fuentes-Delgado, María Consolación Martínez-Saldaña, María Luisa Rodríguez-Vázquez, Miguel Arturo Reyes-Romero, José Luis Reyes-Sánchez, Fernando Jaramillo-Juárez
The urinary increase in γ-GGT activity may be attributed to structural damage on renal proximal cells. GGT is an enzyme located in the brush border membrane of proximal cells of the nephron, which catalyzes the transfer of a γ-glutamyl moiety of GSH to amino acids, dipeptides, and even into GSH itself (McCullough et al. 2013; Tate and Meister 1981; Waring and Moonie 2011). Our histological findings showed a brush border edge loss of proximal cells in MP-exposed rats. Further, histologically edema and positive PAS inclusions were present. Subsequently, a progressive recovery of tubular epithelium with decreased cell edema was observed (at sixth week of MP treatment), and finally, proximal cells recovered the brush border membrane and a normal cytoarchitecture of the renal cortex was detected (8 weeks after MP treatment). These results indicate a recovery process of acute kidney damage (Basile, Anderson, and Sutton 2012; Lattanzio and Kopyt 2009; Solez, Morel-Maroger, and Sraer 1979). In agreement with these findings, Kalender et al. (2007) reported that rats exposed to low doses of MP (0.28 mg/kg per day, orally) showed glomerular atrophy and vascular dilation after 4 weeks of pesticide exposure. Necrosis and edema were observed at 7 weeks of MP treatment and MDA levels increased in kidney tissues. Using a similar model, Khodeary et al. (2009) reported structural damage to the kidney in rats exposed to MP. After 4 weeks of MP exposure, vascular dilation, glomerular atrophy, cloudy swelling in cortical tubules, and few foci hydropic degeneration were observed. At 8 weeks after MP administration, edema, necrosis, interstitial tissue infiltration by inflammatory cells, and glomerular atrophy were detected. Oxidative stress was identified as a mechanism underlying the toxic effect on the kidney. Poovala, Huang, and Salahudeen (1999) reported that OP induced lipid peroxidation, and consequent acute tubular necrosis was associated with ROS generation and lipid peroxidation process.