Related Experiment Video

Updated: Jul 15, 2026

Determining the Toxicity of UV Radiation and Chemicals on Primary and Immortalized Human Corneal Epithelial Cells
09:31

Determining the Toxicity of UV Radiation and Chemicals on Primary and Immortalized Human Corneal Epithelial Cells

Published on: July 22, 2021

Hyperosmolarity-induced apoptosis in human corneal epithelial cells is mediated by cytochrome c and MAPK pathways

Lihui Luo1, De-Quan Li, Stephen C Pflugfelder

  • 1Ocular Surface Center, Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, TX 77030, USA.

Cornea
|April 26, 2007
PubMed
Abstract

Insights

Hyperosmolarity induces apoptosis in human corneal epithelial cells via the cytochrome c pathway. This process is linked to mitogen-activated protein kinase (MAPK) signaling, specifically JNK and ERK pathways.

Area of Science:

  • Cell Biology
  • Ophthalmology
  • Molecular Biology

Background:

  • Hyperosmolarity is a stressor for ocular surface cells.
  • Understanding cell death mechanisms is crucial for ocular health.

Purpose of the Study:

  • To investigate if hyperosmolarity triggers apoptosis in human corneal epithelial cells.
  • To determine the role of cytochrome c-mediated pathways and MAPK activation in this process.

Main Methods:

  • Human corneal epithelial cells were exposed to varying hyperosmolar conditions (450-550 mOsM).
  • Apoptosis was quantified using the ISOL assay.
  • Mitochondrial release of cytochrome c and Smac/DIABLO, caspase-3 activation, and MAPK (JNK/ERK) phosphorylation were assessed via confocal microscopy and Western blotting.
  • Inhibitors for JNK (SB202190) and ERK (PD98059) were used to probe pathway involvement.

Main Results:

  • Hyperosmolarity significantly increased apoptotic cell numbers in a dose-dependent manner.
  • High saline conditions led to cytochrome c and Smac/DIABLO release, caspase-3 activation, and JNK/ERK phosphorylation.
  • Inhibitors blocked hyperosmolarity-induced MAPK activation and apoptosis, with PD98059 also preventing mitochondrial release.

Conclusions:

  • Hyperosmolarity induces apoptosis in human corneal epithelial cells.
  • The cell death mechanism involves the cytochrome c-mediated pathway.
  • JNK and ERK MAPK signaling pathways play a significant role in mediating hyperosmolarity-induced apoptosis.

More Related Videos

Effect of Artificial Tear Formulations on the Metabolic Activity of Human Corneal Epithelial Cells after Exposure to Desiccation06:29

Effect of Artificial Tear Formulations on the Metabolic Activity of Human Corneal Epithelial Cells after Exposure to Desiccation

Published on: May 2, 2020

RNA Interference-based Investigation of the Function of Heat Shock Protein 27 during Corneal Epithelial Wound Healing08:34

RNA Interference-based Investigation of the Function of Heat Shock Protein 27 during Corneal Epithelial Wound Healing

Published on: September 27, 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...
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...
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...
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.
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.
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...