9 research outputs found
Jamming in Embryogenesis and Cancer Progression
The ability of tissues and cells to move and rearrange is central to a broad range of diverse
biological processes such as tissue remodeling and rearrangement in embryogenesis, cell
migration in wound healing, or cancer progression. These processes are linked to a solidlike
to fluid-like transition, also known as unjamming transition, a not rigorously defined
framework that describes switching between a stable, resting state and an active, moving
state. Various mechanisms, that is, proliferation and motility, are critical drivers for the (un)
jamming transition on the cellular scale. However, beyond the scope of these fundamental
mechanisms of cells, a unifying understanding remains to be established. During
embryogenesis, the proliferation rate of cells is high, and the number density is
continuously increasing, which indicates number-density-driven jamming. In contrast,
cells have to unjam in tissues that are already densely packed during tumor
progression, pointing toward a shape-driven unjamming transition. Here, we review
recent investigations of jamming transitions during embryogenesis and cancer
progression and pursue the question of how they might be interlinked. We discuss the
role of density and shape during the jamming transition and the different biological factors
driving it
Differences in cortical contractile properties between healthy epithelial and cancerous mesenchymal breast cells
Cell contractility is mainly imagined as a force dipole-like interaction based on actin stress fibers
that pull on cellular adhesion sites. Here, we present a different type of contractility based on
isotropic contractions within the actomyosin cortex. Measuring mechanosensitive cortical
contractility of suspended cells among various cell lines allowed us to exclude effects caused by
stress fibers. We found that epithelial cells display a higher cortical tension than mesenchymal cells,
directly contrasting to stress fiber-mediated contractility. These two types of contractility can even
be used to distinguish epithelial from mesenchymal cells. These findings from a single cell level
correlate to the rearrangement effects of actomyosin cortices within cells assembled in
multicellular aggregates. Epithelial cells form a collective contractile actin cortex surrounding
multicellular aggregates and further generate a high surface tension reminiscent of tissue
boundaries. Hence, we suggest this intercellular structure as to be crucial for epithelial tissue
integrity. In contrast, mesenchymal cells do not form collective actomyosin cortices reducing
multicellular cohesion and enabling cell escape from the aggregates
Jamming in Embryogenesis and Cancer Progression
The ability of tissues and cells to move and rearrange is central to a broad range of diverse
biological processes such as tissue remodeling and rearrangement in embryogenesis, cell
migration in wound healing, or cancer progression. These processes are linked to a solidlike
to fluid-like transition, also known as unjamming transition, a not rigorously defined
framework that describes switching between a stable, resting state and an active, moving
state. Various mechanisms, that is, proliferation and motility, are critical drivers for the (un)
jamming transition on the cellular scale. However, beyond the scope of these fundamental
mechanisms of cells, a unifying understanding remains to be established. During
embryogenesis, the proliferation rate of cells is high, and the number density is
continuously increasing, which indicates number-density-driven jamming. In contrast,
cells have to unjam in tissues that are already densely packed during tumor
progression, pointing toward a shape-driven unjamming transition. Here, we review
recent investigations of jamming transitions during embryogenesis and cancer
progression and pursue the question of how they might be interlinked. We discuss the
role of density and shape during the jamming transition and the different biological factors
driving it
Jamming in Embryogenesis and Cancer Progression
The ability of tissues and cells to move and rearrange is central to a broad range of diverse
biological processes such as tissue remodeling and rearrangement in embryogenesis, cell
migration in wound healing, or cancer progression. These processes are linked to a solidlike
to fluid-like transition, also known as unjamming transition, a not rigorously defined
framework that describes switching between a stable, resting state and an active, moving
state. Various mechanisms, that is, proliferation and motility, are critical drivers for the (un)
jamming transition on the cellular scale. However, beyond the scope of these fundamental
mechanisms of cells, a unifying understanding remains to be established. During
embryogenesis, the proliferation rate of cells is high, and the number density is
continuously increasing, which indicates number-density-driven jamming. In contrast,
cells have to unjam in tissues that are already densely packed during tumor
progression, pointing toward a shape-driven unjamming transition. Here, we review
recent investigations of jamming transitions during embryogenesis and cancer
progression and pursue the question of how they might be interlinked. We discuss the
role of density and shape during the jamming transition and the different biological factors
driving it
Do antigo ao novo currículo : as experiências dos estágios curriculares do curso de Odontologia da UFRGS na atenção primária em saúde
Do antigo ao novo currículo : as experiências dos estágios curriculares do curso de Odontologia da UFRGS na atenção primária em saúde
Differences in cortical contractile properties between healthy epithelial and cancerous mesenchymal breast cells
Cell contractility is mainly imagined as a force dipole-like interaction based on actin stress fibers
that pull on cellular adhesion sites. Here, we present a different type of contractility based on
isotropic contractions within the actomyosin cortex. Measuring mechanosensitive cortical
contractility of suspended cells among various cell lines allowed us to exclude effects caused by
stress fibers. We found that epithelial cells display a higher cortical tension than mesenchymal cells,
directly contrasting to stress fiber-mediated contractility. These two types of contractility can even
be used to distinguish epithelial from mesenchymal cells. These findings from a single cell level
correlate to the rearrangement effects of actomyosin cortices within cells assembled in
multicellular aggregates. Epithelial cells form a collective contractile actin cortex surrounding
multicellular aggregates and further generate a high surface tension reminiscent of tissue
boundaries. Hence, we suggest this intercellular structure as to be crucial for epithelial tissue
integrity. In contrast, mesenchymal cells do not form collective actomyosin cortices reducing
multicellular cohesion and enabling cell escape from the aggregates
Differences in cortical contractile properties between healthy epithelial and cancerous mesenchymal breast cells
Cell contractility is mainly imagined as a force dipole-like interaction based on actin stress fibers
that pull on cellular adhesion sites. Here, we present a different type of contractility based on
isotropic contractions within the actomyosin cortex. Measuring mechanosensitive cortical
contractility of suspended cells among various cell lines allowed us to exclude effects caused by
stress fibers. We found that epithelial cells display a higher cortical tension than mesenchymal cells,
directly contrasting to stress fiber-mediated contractility. These two types of contractility can even
be used to distinguish epithelial from mesenchymal cells. These findings from a single cell level
correlate to the rearrangement effects of actomyosin cortices within cells assembled in
multicellular aggregates. Epithelial cells form a collective contractile actin cortex surrounding
multicellular aggregates and further generate a high surface tension reminiscent of tissue
boundaries. Hence, we suggest this intercellular structure as to be crucial for epithelial tissue
integrity. In contrast, mesenchymal cells do not form collective actomyosin cortices reducing
multicellular cohesion and enabling cell escape from the aggregates