Abstract
Cellular stress is the basis of a dose-dependent continuum of responses leading to adaptive health or pathogenesis. For all cells, stress leads to reduction in macromolecular synthesis by shared pathways and tissue and stress-specific homeostatic mechanisms. For stem cells during embryonic, fetal, and placental development, higher exposures of stress lead to decreased anabolism, macromolecular synthesis and cell proliferation. Coupled with diminished stem cell proliferation is a stress-induced differentiation which generates minimal necessary function by producing more differentiated product/cell. This compensatory differentiation is accompanied by a second strategy to insure organismal survival as multipotent and pluripotent stem cells differentiate into the lineages in their repertoire. During stressed differentiation, the first lineage in the repertoire is increased and later lineages are suppressed, thus prioritized differentiation occurs. Compensatory and prioritized differentiation is regulated by at least two types of stress enzymes. AMP-activated protein kinase (AMPK) which mediates loss of nuclear potency factors and stress-activated protein kinase (SAPK) that does not. SAPK mediates an increase in the first essential lineage and decreases in later lineages in placental stem cells. The clinical significance of compensatory and prioritized differentiation is that stem cell pools are depleted and imbalanced differentiation leads to gestational diseases and long term postnatal pathologies.
Highlights
Introduction and Summary ofGoals for the ReviewStress is the basis of adaptation and pathology
These stressors consist of nutrient depletion, depletion of ATP [2], low oxygen condition [3,4], oxidative stress [4], heat shock or hyperthermia, high osmotic exposure [5,6], DNA damage caused by exposure to UV radiation or anticancer therapeutics and nuclear envelope stress [7], cold treatment or hypothermia [8], baric stress [9], heavy metal stress [10], changes of cellular metabolism induced by cancerous transformation [11], pro-inflammatory cytokines [12], mechanical stress [13] and stress hormones [14]
We found that hyperosmolar stress causes dose-dependent and time-dependent changes in embryo growth and stem cell accumulation as well as apoptosis, as shown in Figure 2, e.g., 200 mM dose of sorbitol caused stasis of placental trophoblast stem cell (TSC)
Summary
An understanding of stress gives insight into how cells and organisms remain alive and healthy but may mortgage their futures as part of the immediate response to stress. This review will analyze basic areas of the stress response with knowledge derived from adult somatic cell responses and the emerging field of stress responses in stem cells of the early conceptus; embryonic and placental trophoblast stem cells (ESC and TSC, respectively). Stress-induced differentiation is an organismal survival strategy in response to stress exposures which limit stem cell population expansion. This leads to more required differentiated function/cell and increases early lineages while suppressing later ones
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