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Antiviral Drugs as Tools for Nanomedicine
Published in Devarajan Thangadurai, Saher Islam, Charles Oluwaseun Adetunji, Viral and Antiviral Nanomaterials, 2022
In normal cells, during mitosis, cells divide and grow in an interdependent manner, depending on the availability of various stimulants or growth factors and ambient conditions. As the supply is on or off, normal cells switch to proliferation or stop dividing; however, such switch mechanisms are disrupted in transformed cells, due to which they become independent of any signals (Hanahan and Weinberg 2000, 2011). Such transformed cells also lose contact inhibition that is seen in normal cells, where cells stop dividing after attaining a specific threshold. On the contrary, cancer cells do not have any contact inhibition, leading to an uncontrolled mass of cells (Pavel et al. 2018). The life of a normal cell is limited and well-programmed; it dies when function is over, by apoptosis, and is replaced by a new cell. This is due to the limited efficiency of DNA replication, as, at each time, there is a shortening of telomeres. However, cancer cells show the very high activity of telomerase, which keeps restoring the worn-out ends of the telomere, thus granting the cell to proliferate unlimitedly (Trybek et al. 2020). Witsch et al. (2011) has described the stepwise process of cancer development and the role of various growth factors in each step.
Cell Biology for Bioprocessing
Published in Wei-Shou Hu, Cell Culture Bioprocess Engineering, 2020
The vast majority of cells isolated from tissues of mammals are anchorage-dependent, meaning that they require surface adhesion in order to multiply. They are typically isolated from tissues by an enzymatic dissociation of the tissue (Figure 2.1). After dissociation and the removal of undissociated chunks, cells are plated on a compatible surface overlaid with media. The cell clumps in media suspension attach to the surface and gradually some cells grow out from the tissue clumps. Subsequently, cells extend their body length, spread, and begin to multiply. As they begin to cover the entire surface area the growth rate slows down, eventually forming a “monolayer” of cells over the surface. Upon reaching confluence, cell division stops. While the cell bodies of neighboring cells may cross each other, their nuclei never overlap. This is called contact inhibition of cell growth. The contact inhibited cell can be dissociated from the surface by treatment with trypsin. After being plated on a larger surface and provided with fresh medium, cell growth resumes until confluence is again reached. This process can be repeated to expand the population. Each round of detachment and expansion is called a “passage.” The number of cell doublings taking place in each passage is determined by the split ratio, or the ratio of surface area expanded in each passage (see reference 1 for further reading).
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Published in Michael Hehenberger, Zhi Xia, Huanming Yang, Our Animal Connection, 2020
Michael Hehenberger, Zhi Xia, Huanming Yang
A possible mechanism involved in cancer protection may be p16, a tumor suppressor protein, that in humans is encoded by the CDKN2A gene and plays an important role in cell cycle regulation. It prevents cell division once individual cells come into contact (known as “contact inhibition”). The cells of most mammals, including naked mole-rats, undergo contact inhibition via the gene p27, which prevents cellular reproduction at high cell densities. The combination of p16 and p27 in naked mole rat cells is a double barrier to uncontrolled cell proliferation,209 one of the hallmarks of cancer and is known to be implicated in the prevention of several cancers, notably melanoma.
Numerical modelling of osteocyte growth on different bone tissue scaffolds
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2022
Concepción Paz, Eduardo Suárez, Christian Gil, Oscar Parga
The porosity and permeability of a scaffold can be modified using the proliferation of the cells, which invade and reduce the empty space of the porous scaffold structure. This reduction in the space remaining for the appearance of new cells associated with cell growth causes the contact inhibition phenomenon. The cell metabolism slows down as the cell density increases; hence, the cell proliferation greatly reduces or even ceases entirely when a critical cell density is reached (Huang and Ingber 2004). Typical bioreactor operations are carried out under controlled temperature; therefore, in this work, a constant temperature was assumed, and the possible temperature changes due to metabolic reactions were neglected. The different types of bone cells, the shape and size of the cells, cell detachment, and the cell ageing process, were not considered as hypotheses of the model. The density of the culture medium and the pH were considered to be constant (Coletti et al. 2006).
Responsiveness of voltage-gated calcium channels in SH-SY5Y human neuroblastoma cells on micropillar substrates
Published in Journal of Biomaterials Science, Polymer Edition, 2018
Wenxu Wang, Donghuo Zhong, Yu Lin, Rong Fan, Zhengjun Hou, Xiumei Cao, Yubin Ren
Interestingly, the SH-SY5Y cells were deformed significantly to adapt to the topography, but no distinct effect on the proliferation of SH-SY5Y cells was observed. Similar results were also found for SaOs-2 and MG-63 cells [29,30]. Meanwhile, several studies reported that micropillar topography could reduce or stimulate the proliferation rate [31,32]. To understand this phenomenon, two processes that can modulate the proliferation of cells may be useful in understanding this occurrence. One is that the continuation of proliferation needs sufficient spreading, which enhances the sensitivity to soluble mitogens [33,34]. Another is that contact inhibition, which varies by cell types, can be influenced by a number of factors [35]. The proliferation rate of cells cultured in vitro is reduced with contact inhibition [36]; this change is rarely observed in cells in vivo. The two occurrences exhibit a certain relationship with the mechanical signal of the cell microenvironment, and the response of cells to micropillar substrates is a response to the mechanical signal of the substrates. However, no clear trend or hypothesis can be drawn to predict the influence of topography on cell proliferation. It is worth to note that the cellular proliferation was detected using MTS assay that is also a practical approach for assessing the cell viability [37]. The result shows that this PLLA micropillar substrates had no significant cytotoxical effect on cells.