Related Experiment Video

Updated: Aug 18, 2026

Two Methods for Establishing Primary Human Endometrial Stromal Cells from Hysterectomy Specimens
09:15

Two Methods for Establishing Primary Human Endometrial Stromal Cells from Hysterectomy Specimens

Published on: May 23, 2014

Receptorial and mitochondrial apoptotic pathways in normal and neoplastic human endometrium

M Di Paola1, G Loverro, A M Caringella

  • 1Institute of Biomembranes and Bioenergetics, Consiglio Nazionale delle Ricerche, Bari, Italy.

International Journal of Gynecological Cancer : Official Journal of the International Gynecological Cancer Society
|May 11, 2005
PubMed

Insights

Apoptosis pathways are crucial for endometrial tissue homeostasis. Defects in both the receptorial and mitochondrial apoptosis pathways may contribute to endometrial carcinoma development.

Area of Science:

  • Gynecologic Oncology
  • Cellular Biology
  • Molecular Pathology

Background:

  • Apoptosis is vital for human endometrium homeostasis.
  • Dysregulation of apoptosis can lead to neoplastic transformation in reproductive organs.

Purpose of the Study:

  • Investigate the roles of receptorial and mitochondrial apoptosis pathways in normal endometrium and endometrial carcinoma.
  • Measure caspase-3, caspase-8 activities, and cytosolic cytochrome c levels.

Main Methods:

  • Analyzed cytosolic fractions from 12 endometrial carcinomas and 9 normal endometrial specimens.
  • Measured caspase-3 and caspase-8 activities using enzymatic assays.
  • Quantified cytosolic cytochrome c levels via established biochemical methods.

Main Results:

  • Caspase-8 activity was higher in normal secretory endometrium compared to proliferative phase and carcinoma.
  • Elevated cytosolic cytochrome c levels were observed in endometrial carcinoma versus normal secretory endometrium.
  • No significant difference in caspase-3 activity was found between normal and cancerous endometrium.

Conclusions:

  • Normal endometrium utilizes both receptorial and mitochondrial apoptosis pathways.
  • Impaired function in these apoptosis pathways may be implicated in endometrial carcinogenesis.

More Related Videos

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

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.
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...
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...
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...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.
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...