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Updated: Dec 27, 2025

An In-House-Built and Light-Emitting-Diode-Based Photodynamic Therapy Device for Enhancing Verteporfin Cytotoxicity in a 2D Cell Culture Model

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Paraptosis and Photodynamic Therapy: A Progress Report.

¹Department of Pharmacology, Wayne State University School of Medicine, Detroit, MI.

Photochemistry and Photobiology

|March 1, 2020

Summary

Endoplasmic reticulum photodamage initiates paraptosis, a cell death pathway. High-dose damage deviates from the canonical model, with protein cross-linking impairing paraptosis and suggesting alternative cell death routes.

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Area of Science:

Cell Biology
Photobiology
Molecular Biology

Background:

Photodamage to the endoplasmic reticulum (ER) can trigger paraptosis, a distinct cell death pathway.
The canonical paraptosis pathway involves protein synthesis, MAP kinases, and specific biochemical markers.
Autophagy has been reported to inhibit paraptosis.

Purpose of the Study:

To investigate deviations from the canonical paraptosis pathway under high-dose ER photodamage.
To explore the role of protein cross-linking in ER photodamage-induced cell death.
To identify alternative cell death mechanisms at higher photodamage levels.

Main Methods:

Induction of endoplasmic reticulum photodamage in cells.
Assessment of protein synthesis inhibition and cell chilling effects on paraptosis.
Analysis of MAP kinase involvement and autophagy stimulation.
Detection of protein cross-linking, specifically of BiP (binding immunoglobulin protein), using biochemical assays.
Observation of cell death pathways following high-dose photodamage.

Main Results:

Minor ER photodamage (
High-dose ER photodamage (approaching LD90) shows deviations: protein synthesis inhibition and chilling do not prevent paraptosis, and MAP kinases are not involved.
Stimulation of autophagy is not cytoprotective against high-dose ER photodamage.
Substantial cross-linking of BiP was observed at higher photodamage doses, which impaired paraptosis.
Alternative cell death pathways were observed at high photodamage levels.

Conclusions:

High-dose ER photodamage triggers a non-canonical paraptosis pathway.
Protein cross-linking, particularly of BiP, appears to inhibit paraptosis, possibly due to reduced protein mobility.
ER photodamage at high doses can lead to cell death via mechanisms other than canonical paraptosis.