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Related Experiment Video

Updated: Jun 3, 2026

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

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

Published on: January 12, 2024

Hyperglycemia induces apoptosis via CB1 activation through the decrease of FAAH 1 in retinal pigment epithelial

Seul Ki Lim¹, Min Jung Park, Jae Cheong Lim

¹Bio-Therapy Human Resources Center, College of Veterinary Medicine, Chonnam National University, Gwangju, Korea.

Journal of Cellular Physiology

|March 29, 2011

Summary

High glucose downregulates fatty acid amide hydrolase (FAAH) and upregulates CB(1)R in retinal cells, leading to apoptosis. Restoring FAAH 1 expression may offer a novel therapy for diabetic retinopathy.

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Area of Science:

Biochemistry
Cell Biology
Ophthalmology

Background:

Fatty acid amide hydrolase (FAAH) regulates endocannabinoid signaling.
Retinal pigment epithelial (RPE) cells are implicated in diabetic retinopathy pathogenesis.
The role of FAAH in diabetic retinopathy remains unclear.

Purpose of the Study:

To investigate the effect of high glucose (HG) on FAAH and CB(1)R expression in ARPE-19 human RPE cells.
To determine if FAAH 1 overexpression protects against HG-induced cellular damage and apoptosis.

Main Methods:

ARPE-19 and HEK 293 cells were treated with high glucose.
FAAH 1 and CB(1)R expression levels were analyzed via mRNA and protein assays.
Cellular apoptosis, reactive oxygen species generation, and lipid peroxide formation were assessed.
Overexpression of FAAH 1 and CB(1)R blockade were employed.

Main Results:

High glucose downregulated FAAH 1 expression while upregulating CB(1)R expression in ARPE-19 cells.
FAAH 1 overexpression inhibited HG-induced CB(1)R internalization, ROS generation, and lipid peroxidation.
FAAH 1 overexpression, CB(1)R antagonist, and siRNA transfection reduced HG-induced apoptosis.

Conclusions:

High glucose induces apoptosis in RPE cells by upregulating CB(1)R via FAAH 1 downregulation.
Restoring FAAH 1 expression and blocking CB(1)R may represent a therapeutic strategy for diabetic retinopathy.