Maya Ellison
The concept of cellular plasticity has transformed the field of biology, challenging historical conceptions of both the cell and stem cell. Cellular plasticity refers to the ability of cells to reversibly assume different cellular phenotypes, such as transitioning from an epithelial to a mesenchymal phenotype, while still being able to return to their original state. This phenomenon is often regulated by environmental cues triggered during stress and plays a significant role in development, wound repair, and cancer metastasis. In the context of differentiated neurons, cellular plasticity implies the potential for neurons to change their identity and become a different type of cell. This process of de-differentiation or transdifferentiation can be induced experimentally and also occurs naturally in response to tissue injury or cell loss. Recent studies have highlighted the extent to which cell plasticity contributes to tissue homeostasis, with implications for cell-based therapies. While the discovery of cellular plasticity has invigorated the field, most of the molecular drivers behind this phenomenon remain unknown.
| Characteristics | Values |
|---|---|
| Definition | Cell plasticity refers to the ability of cells to reversibly assume different cellular phenotypes, such as transitioning from an epithelial to a mesenchymal phenotype, while still being able to return to their original state. |
| Cellular Potential | Totipotent cells can generate the three embryonic layers as well as the extra-embryonic tissues. Pluripotent cells can contribute to the three embryonic layers. Multipotent cells can generate several but not all cell types. Unipotent cells can generate only one cell type, different from itself. |
| Types of Plasticity | Developmental plasticity, cellular plasticity, synaptic plasticity, and meta-plasticity |
| Driving Factors | Intracellular and extracellular factors, chromatin remodeling, removal of inhibitory factors, and environmental cues |
| Role in Cancer | Cells at an early stage of tumor development are the highest possible candidates to undergo dedifferentiation and transdifferentiation. |
| Role in Neurons | Neural plasticity refers to the ability of nerve cells to modify their behaviors under the influence of microenvironmental factors. |
| Role in Development | Cellular plasticity plays a significant role in development, wound repair, and cancer metastasis. |
| Limitations | Maintaining cellular identity is crucial for normal tissue function, and extreme changes in cell identity can lead to disruptions. |
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What You'll Learn
Neurons can change identity
The concept of cellular plasticity refers to a cell's ability to change its identity. It is a phenomenon that has intrigued biologists for a long time. Cellular plasticity involves the repression of genes associated with the previous cell type and the activation of genes related to the new cell type. This process can be driven by factors inducing a new identity or the loss of factors maintaining the old one.
While the idea of cellular plasticity has been around for a while, recent studies have provided evidence that changes in cell identity are not limited to laboratory settings. Certain adult cells can de-differentiate or transdifferentiate under physiological conditions as part of an organ's normal response to injury or cell loss. For example, neurons became blood cells, and bone marrow cells produced hepatocytes. These findings have significant implications for cell-based therapies and our understanding of tissue homeostasis.
The discovery that terminally differentiated cells can be experimentally coaxed into becoming pluripotent has been a significant development in this field. This reprogramming, which refers to a complete and stable shift, has led to a paradigm shift in our understanding of cellular differentiation. It challenges the historical notion of the process as irreversible and opens up new possibilities for therapeutic interventions.
Neurons, or nerve cells, specifically demonstrate plasticity through their ability to modify their behaviours under the influence of microenvironmental factors. This neuronal plasticity is essential in understanding the development and maturation of the nervous system. Neural plasticity also involves the ability of synapses to change their transmission properties based on previous experiences. While neurons can change their identity, maintaining cellular identity is crucial for normal tissue function. Disruptions in cell identity can lead to issues such as cardiomyocytes stopping contracting or adult neurons ceasing to generate action potentials.
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Plasticity in nerve cells
Neuronal plasticity is driven by neuronotropic factors, which specifically regulate neuronal development. Neural cell cultures are used to identify and purify substances that influence the differentiation and maturation of the nervous system, as well as to study the interdependence between neuronal and glial cells.
Cellular plasticity refers to a cell's ability to change its identity, and it can be experimentally induced. Some differentiated cells have the capacity to de-differentiate or transdifferentiate under physiological conditions as part of an organ's normal injury response. For example, Schwann cells can de-differentiate independently of mitogenic signalling. De-differentiation and transdifferentiation involve the repression of genes associated with the previous cell type and the activation of genes associated with the new cell type. Cells may occupy ''intermediate' identity states during these processes, and such changes can be reversible.
The discovery that differentiated cells can be coaxed to become pluripotent has invigorated the field of cell plasticity. Recent studies have demonstrated that changes in cell identity are not limited to the laboratory, with certain adult cells retaining the capacity to de-differentiate or trans-differentiate under physiological conditions. For instance, neurons have been observed to become blood cells, and bone marrow cells have been observed to produce hepatocytes.
Different types of plasticity are recognised, including synaptic plasticity and meta-plasticity. Synaptic plasticity refers to the ability of a synapse to change its transmission properties according to previous experience. Meta-plasticity refers to a uniform, cell-wide modulation of the modification threshold for synaptic plasticity, controlled by a long-term average of pre- or post-synaptic firing rates.
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Cellular plasticity in cancer development
Cellular plasticity refers to the ability of cells to assume different cellular phenotypes, such as transitioning from an epithelial to a mesenchymal phenotype, while still being able to return to their original state. This phenomenon is often regulated by environmental cues triggered during stress and plays a significant role in development, wound repair, and cancer metastasis.
During cancer progression, tumor cells undergo molecular and phenotypic changes, resulting from microenvironmental cues, stochastic genetic and epigenetic alterations, and/or treatment-imposed selective pressures. These changes contribute to tumor heterogeneity and therapy resistance. Epithelial-mesenchymal plasticity is the best-known case of tumor cell plasticity, but other examples have been identified, often with significant functional consequences.
Cancer cells exploit the malleability of cellular plasticity to their advantage, using it to adjust to unfavorable metabolic environments, evade immune attacks, spread to metastatic sites, and escape the toxic effects of anticancer drugs. For instance, in pancreatic cancer, the degree of chronicity of metaplasia influences cancer risk. Individuals with recurrent or chronic pancreatitis have a much higher risk of developing PDAC, while those with only one or two episodes of uncomplicated acute pancreatitis do not.
Recent studies have also shown that cell plasticity enables tumor cells to change their phenotypic identity in response to drug treatment, without acquiring additional secondary genetic mutations. This has been observed in non-small cell lung cancer (NSCLC), glioblastoma, melanoma, and basal cell carcinoma (BCC).
By studying the underlying biological mechanisms of cell plasticity, researchers hope to develop new strategies for targeting metastasis and therapy resistance in cancer treatment.
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Neural stem cells can give rise to blood cells
Neural stem cells (NSCs) are self-renewing, multipotent cells that generate radial glial progenitor cells, which in turn generate the neurons and glia of the nervous system of all animals during embryonic development. Some neural progenitor stem cells persist in highly restricted regions in the adult vertebrate brain and continue to produce neurons throughout life.
NSCs have the potential to give rise to offspring cells that grow and differentiate into neurons and glial cells (non-neuronal cells that insulate neurons and enhance the speed at which neurons send signals). NSCs are stimulated to begin differentiation via exogenous cues from the microenvironment, or stem cell niche. Some neural cells are migrated from the SVZ along the rostral migratory stream, which contains a marrow-like structure with ependymal cells and astrocytes when stimulated. The ependymal cells and astrocytes form glial tubes used by migrating neuroblasts. The astrocytes in the tubes provide support for the migrating cells as well as insulation from electrical and chemical signals released from surrounding cells.
In the central nervous system (CNS), precise communication between the vascular and neural compartments is essential for proper development and function. Recent studies demonstrate that certain neuronal populations secrete various molecular cues to regulate blood vessel growth and patterning in the spinal cord and brain during development. The vasculature is now emerging as a critical component that regulates stem cell niches during neocortical development, as well as during adulthood.
While neural stem cells have not been found to give rise to blood cells, there has been research into hematopoietic stem cells (HSCs), which usually differentiate into blood cells but can also be transdifferentiated into neural lineages. These HSCs can be found in bone marrow, umbilical cord blood, and peripheral blood cells. Interestingly, these cells have been found to be spontaneously mobilized by certain types of strokes and can also be further mobilized by granulocyte colony-stimulating factor (G-CSF).
Cell plasticity refers to the ability of cells to reversibly assume different cellular phenotypes, such as transitioning from an epithelial to a mesenchymal phenotype, while still being able to return to their original state. Cellular plasticity involves the repression of genes associated with the previous cell type and the activation of genes associated with the new cell type. Cells may occupy 'intermediate' identity states while undergoing de-differentiation or transdifferentiation. Such changes can be reversible and are driven by factors that induce a new identity or the loss of inhibitory factors that maintain the old identity.
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Cell plasticity in wound repair
Cell plasticity refers to the ability of cells to assume different cellular phenotypes, such as transitioning from an epithelial to a mesenchymal phenotype, while still being able to return to their original state. This phenomenon is often regulated by environmental cues triggered during stress and plays a significant role in development, wound repair, and cancer metastasis.
Wound healing is a complex, dynamic process supported by a myriad of cellular events that must be tightly coordinated to efficiently repair damaged tissue. A skin wound, for example, requires several cell lineages to exhibit considerable plasticity as they migrate towards and over the site of damage to contribute to repair. The keratinocytes that re-epithelialize the tissue, the dermal fibroblasts, and potentially other mesenchymal stem cell populations that repopulate damaged connective tissue are all part of this process. These cells are 'dynamic' in that they are activated by immediate wound cues, they reprogram to adopt cell behaviors essential for repair, including migration, and finally, they must resolve.
Cell plasticity has been observed in differentiated cells in wound repair and tumorigenesis in the skin and intestine. In the skin, for example, stem cell plasticity enables hair regeneration following Lgr5(+) cell loss. In the stomach and pancreas, studies have identified and begun to characterize the roles of regenerative cellular plasticity. This includes the concept of paligenosis, a conserved cellular program that may allow mature cells to become regenerative.
The discovery that terminally differentiated cells can be coaxed experimentally to become pluripotent has invigorated the field of cell plasticity. Recent studies have demonstrated that changes in cell identity are not limited to the laboratory, as certain adult cells retain the capacity to de-differentiate or trans-differentiate under physiological conditions as part of an organ’s normal injury response.
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Frequently asked questions
Cellular plasticity refers to the ability of cells to reversibly assume different cellular phenotypes, such as transitioning from an epithelial to a mesenchymal phenotype, while still being able to return to their original state.
Yes, differentiated neurons can exhibit cellular plasticity. Some differentiated cells have the capacity to de-differentiate or transdifferentiate under physiological conditions as part of a normal response. For example, neurons have become blood cells, and bone marrow cells have produced hepatocytes.
Cellular plasticity has therapeutic potential, helping to attract research funding and private investment into the stem cell field. It also has implications for cell-based therapy and contributes to tissue homeostasis.
