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Cell injury and apoptosis
1Faculty of Medicine, Memorial University of Newfoundland, St. John's, Canada.
Abstract:
Various forms of cellular injury, whether induced by immune effector cells, aberrant metabolic processes, chemotherapeutic drugs or temperature shifts, result in common morphological changes consisting of the formation and shedding of membrane vesicles from the injured cell surfaces, i.e., apoptosis. This dynamic cell surface membrane behavior appears to be dependent on the disruption of cytoplasmic microtubules. Concomitant with the altered cell surface morphology, certain physiological and biochemical events have been found to be associated with cell injury. These include changes in membrane permeability, elevated oxygen consumption rates and nuclear DNA fragmentation. However, it remains to be experimentally established which of these biological changes defines a state of irreparable cell injury and/or programmed cell death (PCD). Selective cell injury and death is the goal of many therapeutic modalities aimed at the destruction of malignant cells. On the other hand, prevention of cell injury is desirable in autoimmune diseases such as systemic lupus erythematosus, thyroiditis, insulin dependent diabetes and many others. Injury to the vascular endothelium may play a role not only in thrombosis, atherosclerosis and hypertension, but may also provide the avenues for the metastasis of malignant cells. The objective of the present review is to compare and evaluate the cell injury process induced by effector lymphocytes with that caused by low temperature. The latter mimics most, if not all, the currently known criteria of immune effector cell mediated PCD of target tumor cells.
Insights
Cellular injury, including apoptosis, involves membrane vesicle shedding and is linked to microtubule disruption. Low temperatures mimic immune cell-induced programmed cell death, offering insights into cell death mechanisms.
Area of Science:
- Cell Biology
- Immunology
- Pathology
Background:
- Cellular injury from various stimuli causes common morphological changes, including apoptosis.
- Cell surface membrane dynamics, like vesicle shedding, are crucial during cell injury.
- Physiological changes such as altered membrane permeability and DNA fragmentation accompany cell injury.
Purpose of the Study:
- To compare cell injury induced by effector lymphocytes with that caused by low temperature.
- To evaluate if low temperature mimics immune-mediated programmed cell death (PCD).
- To understand the mechanisms defining irreparable cell injury and PCD.
Main Methods:
- Comparative analysis of cellular injury mechanisms.
- Evaluation of morphological and physiological changes in injured cells.
- Assessment of low temperature as a model for immune-mediated cell death.
Main Results:
- Cellular injury, regardless of the inducer, results in common morphological changes like apoptosis.
- Disruption of cytoplasmic microtubules appears critical for cell surface membrane changes during injury.
- Low temperature exposure effectively mimics key criteria of immune effector cell-mediated PCD.
Conclusions:
- Low temperature serves as a valuable experimental model for studying immune-mediated programmed cell death.
- Understanding cell injury mechanisms is vital for therapeutic strategies targeting cancer and autoimmune diseases.
- Further research is needed to pinpoint the definitive markers of irreparable cell injury and PCD.