Aggregates formed from cells that can descend from different lineages are thought to have more genetic conflict and thus reach less complexity. There are complementary ways to tackle this problem. Some sources suggest that genetic homogeneity is not a necessary condition for cell differentiation for example in the case of D. From the DPMs framework we could speculate than some differences between aggregates and organisms arising from incomplete division might be due to the dynamic differences between clusters that result from cells that become coupled in a single and relatively fast event aggregation vs.
Similarly, the relationship between size of the aggregate and cell differentiation has been well documented Bonner, In the context of the cooperation-defection framework, it has been suggested that once a mass of undifferentiated cells reaches a threshold size, division of labor becomes beneficial for the group even if it implies that some of the cell types will have relatively low fitness, leading to or maintaining cell differentiation Michod, However, another explanation based on the dynamical properties of coupled cells is also possible; Kaneko has suggested that in larger aggregates of coupled cells, more microenvironments of nutrient concentration or signals can emerge from cell-to-cell and cell-medium interactions, which in turn bias the cellular fates and yield more cell types Furusawa and Kaneko, Finally, it is worth noting that our work and discussion focuses on the process of cellular differentiation and patterning in emerging multicellular organisms and that any extrapolation to other biological or social scales are beyond the scope of our model though it would be interesting to address how the coupling of different dynamic mechanisms could change our understanding of collective organization at other scales.
We have pursued a modeling approach based on the DPM framework to address one of the questions we consider central in evolutionary developmental biology: the origin of cell differentiation and patterning in the transition to multicellularity. This approach relies on different assumptions than the cooperation-defection framework on the problem of cell differentiation and provides new working hypotheses, complemented with dynamical mathematical modeling.
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A variety of factors can trigger cell death in a tissue. For example, the process of apoptosis, or programmed cell death, selectively removes damaged cells — including those with DNA damage or defective mitochondria. During apoptosis, cellular proteases and nucleases are activated, and cells self-destruct. Cells also monitor the survival factors and negative signals they receive from other cells before initiating programmed cell death. Once apoptosis begins, it proceeds quickly, leaving behind small fragments with recognizable bits of the nuclear material.
Specialized cells then rapidly ingest and degrade these fragments, making evidence of apoptosis difficult to detect. Figure 2 : Different cell types in the mammalian gut The gut contains a mixture of differentiated cells and stem cells. The a intestine, b esophagus, and c stomach are shown. Through asymmetric division, quiescent stem cells d probably give rise to more rapidly dividing active stem cells, which then produce progenitor cells while losing their multipotency and ability to proliferate.
All these progeny cells have defined positions in the different organs. To maintain its function and continue to produce new stem cells, a stem cell can also divide into and produce more stem cells at the same position symmetric division.
Stem cells in gastroenterology and hepatology. All rights reserved. Figure Detail Tissue function depends on more than cell type and proper rates of death and division: It is also a function of cellular arrangement.
Both cell junctions and cytoskeletal networks help stabilize tissue architecture. For instance, the cells that make up human epithelial tissue attach to one another through several types of adhesive junctions.
Characteristic transmembrane proteins provide the basis for each of the different types of junctions. At these junctions, transmembrane proteins on one cell interact with similar transmembrane proteins on adjacent cells. Special adaptor proteins then connect the resulting assembly to the cytoskeleton of each cell. The many connections formed between junctions and cytoskeletal proteins effectively produces a network that extends over many cells, providing mechanical strength to the epithelium.
The gut endothelium — actually an epithelium that lines the inner surface of the digestive tract — is an excellent example of these structures at work. Here, tight junctions between cells form a seal that prevents even small molecules and ions from moving across the endothelium.
As a result, the endothelial cells themselves are responsible for determining which molecules pass from the gut lumen into the surrounding tissues. Meanwhile, adherens junctions based on transmembrane cadherin proteins provide mechanical support to the endothelium.
These junctions are reinforced by attachment to an extensive array of actin filaments that underlie the apical — or lumen-facing — membrane. These organized collections of actin filaments also extend into the microvilli , which are the tiny fingerlike projections that protrude from the apical membrane into the gut lumen and increase the surface area available for nutrient absorption.
Additional mechanical support comes from desmosomes , which appear as plaque-like structures under the cell membrane, attached to intermediate filaments. In fact, desmosome-intermediate filament networks extend across multiple cells, giving the endothelium sheetlike properties.
In addition, within the gut there are stem cells that guarantee a steady supply of new cells that contribute to the multiple cell types necessary for this complex structure to function properly Figure 2.
The extracellular matrix ECM is also critical to tissue structure, because it provides attachment sites for cells and relays information about the spatial position of a cell. The ECM consists of a mixture of proteins and polysaccharides produced by the endoplasmic reticula and Golgi apparatuses of nearby cells. Once synthesized, these molecules move to the appropriate side of the cell — such as the basal or apical face — where they are secreted.
Final organization of the ECM then takes place outside the cell. To understand how the ECM works, consider the two very different sides of the gut endothelium. One side of this tissue faces the lumen, where it comes in contact with digested food.
Under normal physiological conditions, cells that have differentiated into a specific, stable type are generally impossible to reverse to undifferentiated state or become other types. Cell differentiation is plastic, and the differentiated cells re-enter the undifferentiated state or transdifferentiate into another type of cell under special conditions.
Embryonic stem cells ES cells have the potential to develop into different types of cells. Under suitable conditions in vitro , they can proliferate in an undifferentiated state, providing a source of cells for the research and application of ES cells.
The mouse embryonic stem cells treated with retinoic acid will differentiate into neural progenitor cells and then treat with Shh specific small molecule antagonist Hh-Ag 1. Takahashi et al found that ascorbic acid can effectively enhance the differentiation of embryonic stem cells into cardiomyocytes. Wu et al. Hironori et al. Of course, due to the existence of immunocompatibility issues, the safety of embryonic stem cell transplantation needs to be a comprehensive, objective and in-depth evaluation.
Bone marrow stromal cells MSCs are derived from mesoderm and can differentiate into mesoderm cells such as osteoblasts, chondrocytes, myoblasts, tendon cells, adipocytes, and stromal cells under certain induction conditions; it can differentiate into neuroblast cells of the ectoderm and hepatic oval cells of the endoderm. Due to its wide source of materials and the low degree of immune rejection during transplantation, it is a target cell for cell replacement therapy with the good clinical application.
Many research groups conducted in vitro differentiation experiments of MSCs under in vitro culture conditions. Woodbury et al. Deng et al. MSCs can differentiate into osteoblasts under the induction of dexamethasone, sodium 8-glycerophosphate and vitamin C.
Dexamethasone can regulate gene expression in differentiated cells and promote the transformation into osteoblasts by enhancing the affinity of its receptors to genomic target sequences. It is an essential component of osteogenic differentiation of MSCs in vitro , and vitamin C is also an important inducer. It is found that both 5-azacytidine and 5-azdeoxycytidine can promote MSCs to muscle differentiation.
Currently, inducers that induce differentiation of MSCs into neuron-like cells are mainly antioxidants and calcium channel blockers. Antioxidants may bind to certain specific receptors on the surface of MSCs, thereby initiating one or more signaling pathways that ultimately differentiate into neurons. For example, MSCs treated with the small molecule compound D showed significant morphological changes, demonstrating that antioxidant D can induce MSCs to differentiate into neuron-like cells.
Most of the experiments in recent years have used some antioxidants, and the traditional Chinese medicine Salvia miltiorrhiza contains various antioxidant components such as tanshinone and total salvianolic acid. Qingtao et al.
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