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Published on: March 22, 2015
Methylglyoxal induces apoptosis mediated by reactive oxygen species in bovine retinal pericytes
Jaetaek Kim1, Jang-Won Son, Jeong-An Lee
1Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, Chung-Ang University, Seoul, Korea. jtkim@cau.ac.kr
Abstract:
One of the histopathologic hallmarks of early diabetic retinopathy is the loss of pericytes. Evidences suggest that the pericyte loss in vivo is mediated by apoptosis. However, the underlying cause of pericyte apoptosis is not fully understood. This study investigated the influence of methylglyoxal (MGO), a reactive alpha-dicarbonyl compound of glucose metabolism, on apoptotic cell death in bovine retinal pericytes. Analysis of internucleosomal DNA fragmentation by ELISA showed that MGO (200 to 800 microM) induced apoptosis in a concentration-dependent manner. Intracellular reactive oxygen species were generated earlier and the antioxidant, N-acetyl cysteine, inhibited the MGO-induced apoptosis. NF-kappaB activation and increased caspase-3 activity were detected. Apoptosis was also inhibited by the caspase-3 inhibitor, Z-DEVD-fmk, or the NF-kappaB inhibitor, pyrrolidine dithiocarbamate. These data suggest that elevated MGO levels observed in diabetes may cause apoptosis in bovine retinal pericytes through an oxidative stress mechanism and suggests that the nuclear activation of NF-kappaB are involved in the apoptotic process.
Insights
Methylglyoxal (MGO) induces apoptosis in bovine retinal pericytes via oxidative stress. This process involves reactive oxygen species generation, NF-kappaB activation, and caspase-3 activity, contributing to diabetic retinopathy.
Area of Science:
- Ophthalmology
- Cell Biology
- Biochemistry
Background:
- Diabetic retinopathy is characterized by pericyte loss, a process linked to apoptosis.
- The precise mechanisms driving pericyte apoptosis in diabetes remain unclear.
Purpose of the Study:
- To investigate the role of methylglyoxal (MGO) in inducing apoptosis in bovine retinal pericytes.
- To elucidate the molecular pathways involved in MGO-induced pericyte apoptosis.
Main Methods:
- Bovine retinal pericytes were treated with varying concentrations of MGO.
- Apoptosis was assessed via DNA fragmentation (ELISA).
- Reactive oxygen species (ROS) generation, NF-kappaB activation, and caspase-3 activity were measured.
Main Results:
- MGO induced concentration-dependent apoptosis in pericytes.
- MGO treatment led to increased intracellular ROS, NF-kappaB activation, and caspase-3 activity.
- Antioxidants (N-acetyl cysteine) and inhibitors (Z-DEVD-fmk, pyrrolidine dithiocarbamate) attenuated MGO-induced apoptosis.
Conclusions:
- Elevated MGO levels in diabetes may induce retinal pericyte apoptosis through oxidative stress.
- NF-kappaB activation and caspase-3 are key mediators in the MGO-induced apoptotic pathway.
