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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...
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 IlI: Cellular Death01:11

Cellular Injury IlI: Cellular Death

Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...
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: Jul 18, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

Intestinal cell apoptosis and Bcl-2 expression.

Y Shaposhnikov1, Y Maheshwari, D E Sykes

  • 1Division of Gastroenterology, Hepatology and Nutrition, Department of Medicine, State University of New York, Buffalo.

Cell Death and Differentiation
|January 1, 1996
PubMed
Summary

Programmed cell death (apoptosis) is a normal process in intestinal cells. Increased Bcl-2 expression may protect proliferative enterocytes from stress-induced apoptosis.

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Related Experiment Videos

Last Updated: Jul 18, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

Examining BCL-2 Family Function with Large Unilamellar Vesicles
08:35

Examining BCL-2 Family Function with Large Unilamellar Vesicles

Published on: October 5, 2012

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
12:55

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Gastroenterology

Background:

  • Programmed cell death, or apoptosis, is a fundamental biological process.
  • The Bcl-2 proto-oncogene plays a key role in regulating apoptosis.
  • Enterocytes and proliferative crypt cells undergo apoptosis under normal and stress conditions.

Purpose of the Study:

  • To investigate the relationship between enterocyte apoptosis and Bcl-2 expression in the rat intestine.
  • To evaluate Bcl-2 transcript levels and DNA fragmentation in different intestinal cell fractions and cell cultures.

Main Methods:

  • Analysis of DNA fragmentation in isolated rat intestinal cell nuclei.
  • Quantification of Bcl-2 mRNA levels in rat enterocyte fractions and IEC tissue culture cells.
  • Induction of apoptosis in IEC cells via long-term confluent culture and serum deprivation.

Main Results:

  • Low levels of DNA fragmentation were observed in all enterocyte fractions, including crypt cells.
  • Detectable DNA fragmentation in IEC cells occurred under long-term culture conditions.
  • Bcl-2 mRNA was absent in isolated rat intestinal cells but present in IEC cells, increasing with serum deprivation and culture duration.

Conclusions:

  • Increased Bcl-2 expression may be crucial for the survival of proliferative enterocytes facing stress.
  • Bcl-2 regulation might be a protective mechanism against apoptosis in intestinal epithelial cells.
  • Further research into Bcl-2's role in intestinal cell homeostasis is warranted.