Related Experiment Video

Updated: Jul 14, 2026

Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments
08:55

Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments

Published on: April 24, 2020

Regulation of cell death and survival pathways in experimental glaucoma

Hani Levkovitch-Verbin1, Noga Harizman, Rima Dardik

  • 1Sam Rothberg Ophthalmic Molecular Biology Laboratory, Goldschleger Eye Institute, Sheba Medical Center, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Hashomer 52621, Israel. halevko@hotmail.com

Experimental Eye Research
|June 26, 2007
PubMed

Insights

Experimental glaucoma in rats reveals that retinal ganglion cell death involves both pro-apoptotic (MAP kinase, caspase-3) and pro-survival (PI3-Kinase/Akt, p-ERK) pathways activating at different times.

Area of Science:

  • Ophthalmology
  • Neuroscience
  • Molecular Biology

Background:

  • Glaucoma is a leading cause of irreversible blindness.
  • Understanding the molecular mechanisms of retinal ganglion cell death is crucial for developing neuroprotective therapies.

Purpose of the Study:

  • To investigate the temporal activation of cell death and survival pathways in experimental glaucoma.
  • To elucidate the roles of the MAP kinase pathway, caspase-3, and PI3-Kinase/Akt signaling in glaucoma pathogenesis.

Main Methods:

  • Experimental glaucoma was induced in Wistar rats using translimbal photocoagulation.
  • Protein levels of caspase-3, p-AKT, and MAP kinase pathway members (p-SAPK/JNK, p-P38, p-ATF-2, p-ERK) were assessed using immunohistochemistry and Western blotting at various time points.

Main Results:

  • Elevated caspase-3 levels were observed from day 15 to day 30.
  • Significant activation of MAP kinase pathway members, including p-SAPK/JNK, p-P38, and p-ATF-2, occurred at different time points.
  • Pro-survival proteins p-ERK and p-Akt were detected early but returned to baseline at later time points.

Conclusions:

  • Retinal ganglion cell death in experimental glaucoma is a complex process involving the coordinated activation of multiple pro-apoptotic and pro-survival signaling pathways.
  • The differential temporal activation of these pathways suggests potential therapeutic windows for intervention.

More Related Videos

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation08:30

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation

Published on: March 12, 2016

Experimental Glaucoma Induced by Ocular Injection of Magnetic Microspheres06:35

Experimental Glaucoma Induced by Ocular Injection of Magnetic Microspheres

Published on: February 2, 2015

Related Concept Videos

Glaucoma: Overview01:25

Glaucoma: Overview

Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...
Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...
Angle Closure Glaucoma: Treatment01:28

Angle Closure Glaucoma: Treatment

Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...
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...