Related Experiment Video

Updated: Jun 19, 2026

An Assay to Detect Protection of the Retinal Vasculature from Diabetes-Related Death in Mice
04:36

An Assay to Detect Protection of the Retinal Vasculature from Diabetes-Related Death in Mice

Published on: January 12, 2024

Retinal ischemia-induced apoptosis is associated with alteration in Bax and Bcl-x(L) expression rather than

Nathalie Produit-Zengaffinen1, Constantin J Pournaras, Daniel F Schorderet

  • 1Institute for Research in Ophthalmology, Sion, Switzerland. nathalie.produit@irovision.ch

Molecular Vision
|October 29, 2009
PubMed
Abstract

Insights

Mitochondrial apoptotic pathway molecules shift towards cell death during late-phase recovery from retinal ischemia/reperfusion. This shift, marked by increased Bax:Bcl-x(L) ratios and caspase-3, contributes to retinal damage progression.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Molecular Biology

Background:

  • Apoptosis plays a critical role in retinal cell death following ischemia.
  • The kinetics and specific signaling pathways contributing to this process remain incompletely understood.

Purpose of the Study:

  • To investigate the expression changes of key molecules in the mitochondrial apoptotic pathway after retinal ischemia/reperfusion.
  • To elucidate the contribution of these molecular changes to the progression of retinal damage.

Main Methods:

  • Retinal ischemia was induced in a rodent model by elevating intraocular pressure.
  • Expression of Bax, Bak, Bcl-2, Bcl-x(L), caspase-3, and caspase-7 was analyzed at early (3h) and late (24h) phases post-reperfusion using qPCR and Western blot.

Main Results:

  • Early phase: Bcl-2 family mRNA decreased, while protein levels of Bcl-2 and Bcl-x(L) increased; ratios remained stable.
  • Late phase: Bax:Bcl-2 and Bax:Bcl-x(L) ratios increased at both mRNA and protein levels.
  • Caspase-3 expression increased, while caspase-7 decreased in the late phase.

Conclusions:

  • Bcl-2 family members exhibit differential regulation during early and late phases of retinal ischemia recovery.
  • A shift in the Bax:Bcl-x(L) ratio towards apoptosis occurs in the late phase.
  • Upregulation of caspase-3 reinforces this pro-apoptotic shift, contributing to retinal damage.

More Related Videos

Quantification of Immunostained Caspase-9 in Retinal Tissue05:18

Quantification of Immunostained Caspase-9 in Retinal Tissue

Published on: July 25, 2022

A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure07:37

A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure

Published on: July 14, 2016

Related Concept Videos

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...
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 IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...