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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 extension and branching of neurites (thin projections from the cell body, including axons and dendrites) in culture can be similarly regulated by the rigidity of the cellular microenvironment (Figure 24.2) [43–46]; substrates that are either much softer or much stiffer than the normal brain microenvironment often do not support robust neurite extension in vitro, although the details of this relationship appear to depend upon the cell source and substrate geometry and composition. This correlation may have implications for neuroregeneration and tumorigenesis; for example, it was recently proposed that the softening of reactive astrocytes following mechanical injury may provide a compliant, brain-like mechanical substrate that promotes neurite extension [50]. We recently showed that the potency with which retinoic acid can induce neurite extension, reduce proliferation and suppress N-Myc expression in neuroblastoma tumor cells all depend strongly on ECM stiffness [51]. Given the substantial mechanical stress exerted by neurites on adhesive substrates [52–54], this phenomenon is likely related to the capacity of the underlying substrate to support generation of contractile forces within elongating projections. Interestingly, neurites have been elicited in vitro by direct application of tensile forces with glass microneedles, where active elongation is observed when tension is maintained above a threshold value, and active retraction is observed when tension is released [53–56]. Follow-up studies using magnetic beads to apply external loads to elongating neurites showed that forces on the order of 1.5 nN are required to elicit neurites, and that force-induced neurite initiation and elongation appears to be a highly conserved property that is largely independent of cell age and synaptic phenotype [57,58].
Buthionine sulfoximine and chemoresistance in cancer treatments: a systematic review with meta-analysis of preclinical studies
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Camila dos Reis Oliveira, Joedna Cavalcante Pereira, Andressa Barros Ibiapina, Italo Rossi Roseno Martins, João Marcelo de Castro e Sousa, Paulo Michel Pinheiro Ferreira, Felipe Cavalcanti Carneiro da Silva
Neuroblastoma cell lines SMS-KANR (BSO-sensitive neuroblastoma cell line) and SK-N-RA (BSO-resistant neuroblastoma cell line), with and without N-MYC gene overexpression (oncogenic driver), respectively, were treated with 500 µM D,L-BSO for 72 hr (Anderson et al. 1999). Flow cytometry and DNA fragment labeling demonstrated more than 90% of apoptotic SMS-KANR cells, while SK-N-RA presented less than 10% of apoptotic cells. Interestingly, GSH depletion produced by D, L-BSO differed between cell lines and was not correlated with the degree of cytotoxicity initiated by D,L-BSO (Anderson et al. 1999).
Applications and hazards associated with carbon nanotubes in biomedical sciences
Published in Inorganic and Nano-Metal Chemistry, 2020
Ali Hassan, Afraz Saeed, Samia Afzal, Muhammad Shahid, Iram Amin, Muhammad Idrees
Spermatogenesis may also be affected by the environmental toxicants.[96] The number of such environmental effects caused by toxicants like the nanoparticles is continuously increasing and is known to affect many organs including the testis.[67,97,98] When the nanoparticles enter the systematic circulation, they can easily penetrate many capillaries, epithelia, and biological membranes and they can comprehensively alter functioning of any animal cell.[99,100] It is said that the nanoparticles not only can cross the blood-brain barrier but can also evade the blood-testis barrier and get distributed in the gonads.[97,101,102] Spermatogonial stem cells (SSCs) are the progenitors that are necessary for differentiation and self-renewal of the sperm cells and maintaining permanent spermatogenesis. These stem cells are controlled and regulated partly by a small peptide GDNF which was first discovered in the brain cells.[103,104] The GDNF belongs to the transforming growth factor-β which works on its specific cell by binding to its receptor c-Ret and a co-receptor GFR-α releasing secondary messengers. Removing out any of these factors can cause the decline in the SSCs proliferation and activity. GDNF phosphorylates the c-Ret and Src kinase family proteins (SFK) the phosphorylation of SFK is very significant in maintaining the SSC population. SFK causes the phosphorylation of the PI3K and AKT and all this cascade of reaction ends at the N-Myc which is a transcription factor which was first said to be the tumor inducer but now said to have role in the maintaining the SSC populations.[74,104–107]