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Related Concept Videos

Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...

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Related Experiment Video

Updated: Jun 24, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Apoptosis and gene expression after TBI.

Jan Dressler1, Raghu Vemuganti

  • 1Institute of Legal Medicine, Technical University Dresden, Fetscherstrasse 74, D-01307 Dresden, Germany. Jan.Dressler@tu-dresden.de

Legal Medicine (Tokyo, Japan)
|March 14, 2009
PubMed
Summary

Traumatic brain injury (TBI) alters gene expression in the central nervous system (CNS). Understanding these genetic changes, including necrosis and apoptosis, aids in estimating TBI wound age for legal medicine.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Forensic Medicine

Background:

  • Central nervous system (CNS) function relies on precise gene expression.
  • Traumatic brain injury (TBI) can cause neuronal death and dysfunction.
  • Altered gene expression is a potential mechanism underlying TBI-induced damage.

Purpose of the Study:

  • To analyze gene expression changes in the CNS following TBI.
  • To investigate the role of specific genes in TBI pathology.
  • To explore the utility of TBI-induced genetic changes for forensic applications.

Main Methods:

  • Utilized a CNS-specific GeneChip for comprehensive gene expression profiling.
  • Employed real-time polymerase chain reaction (PCR) for quantitative gene expression analysis.

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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Establishing Cell Lines Overexpressing DR3 to Assess the Apoptotic Response to Anti-mitotic Therapeutics
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  • Examined markers of necrosis and apoptosis.

    • Main Results:

    • Identified significant alterations in gene expression patterns post-TBI.
    • Observed molecular signatures indicative of both necrosis and apoptosis.
    • Correlated gene expression changes with TBI pathology.

    Conclusions:

    • Gene expression profiling provides insights into TBI mechanisms.
    • Necrosis and apoptosis markers identified in TBI can inform wound age estimation.
    • This research contributes to the application of molecular biology in legal medicine.