Glycolaldehyde, an Advanced Glycation End Products Precursor, Induces Apoptosis via ROS-Mediated Mitochondrial Dysfunction in Renal Mesangial Cells

Glycolaldehyde (GA) is a reducing sugar and a precursor of advanced glycation end products (AGEs). The role of precursor and precursor-derived AGEs in diabetes and its complications have been actively discussed in the literature. This study aimed to elucidate the mechanism of GA-induced apoptosis in...

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Bibliographic Details
Published in:Antioxidants 2022-05, Vol.11 (5), p.934
Main Authors: Gu, Min Ji, Hyon, Ju-Youg, Lee, Hee-Weon, Han, Eun Hee, Kim, Yoonsook, Cha, Youn-Soo, Ha, Sang Keun
Format: Article
Language:English
Subjects:
advanced glycation end products
Advanced glycosylation end products
Age
Alzheimer's disease
Antibodies
Apoptosis
Bcl-2 protein
Caspase-3
Chronic illnesses
Cytochrome c
Cytotoxicity
Diabetes
Diabetes mellitus
Diabetic neuropathy
DNA fragmentation
Flow cytometry
Glycolaldehyde
Glycosylation
Immunoblotting
Immunomodulation
Kidneys
Membrane potential
mesangial cell
Mesangial cells
Metabolism
Mitochondria
mitochondrial dysfunction
Oxidative stress
Pathogenesis
Penicillin
Proteins
Reactive oxygen species
Renal function
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Summary:Glycolaldehyde (GA) is a reducing sugar and a precursor of advanced glycation end products (AGEs). The role of precursor and precursor-derived AGEs in diabetes and its complications have been actively discussed in the literature. This study aimed to elucidate the mechanism of GA-induced apoptosis in renal cells. Immunoblotting results showed that GA (100 μM) caused cytotoxicity in murine renal glomerular mesangial cells (SV40 MES 13) and induced apoptosis via major modulators, decreasing Bcl-2 and increasing Bax, cytochrome c, and cleaved caspase-3/-9 expression. GA-derived AGE accumulation and receptor for AGE (RAGE) expression increased in mesangial cells; however, cells that were cotreated with aminoguanidine (AG) showed no increase in GA-derived AGE concentration. Furthermore, reactive oxygen species (ROS) production was increased by GA, while AG inhibited AGE formation, leading to a decrease in ROS levels in mesangial cells. We evaluated apoptosis through fluorescence-activated cell sorting, and used TUNEL staining to study DNA fragmentation. Additionally, we measured ATP generation and used MitoTracker staining to access changes in mitochondrial membrane potential. This study showed that GA increased AGE concentration, RAGE expression, and excessive ROS generation, leading to renal mesangial cell damage via GA-induced apoptosis pathway caused by mitochondrial dysfunction.
ISSN:2076-3921
2076-3921
DOI:10.3390/antiox11050934