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Cited by 97Advanced Glycation End Products researchGlycosylation and Glycoproteins ResearchNitric Oxide and Endothelin Effects

Advanced glycation endproduct induces ROS accumulation, apoptosis, MAP kinase activation and nuclear O-GlcNAcylation in human cardiac myocytes

Li, Shi-Yan, Sigmon, Valerie K., Babcock, Sara A., Ren, Jun·2007·Life Sciences
DOI 10.1016/j.lfs.2006.11.035
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Abstract

Accumulation of advanced glycation endproduct (AGE) has been implicated in the pathogenesis of diabetic complications. However, the precise role and mechanism behind AGE-associated diabetic heart injury are not fully clear. This study was designed to evaluate the effect of AGE on accumulation of reactive oxygen species (ROS), apoptosis, mitogen-activated protein kinase (MAPK) activation and nuclear O-GlcNAcylation in fetal human cardiac myocytes. Myocytes were maintained for 24-72 h in a defined culture medium containing high glucose, the AGE carbon precursor methylglyoxal (MG), and MG-AGE derived from MG and bovine serum albumin (BSA). Generation of ROS was detected by 5-(6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate. Apoptosis was evaluated by caspase-3 activity and quantitative DNA fragmentation. Both high glucose (25.5 mM) and MG (200 microM) significantly enhanced ROS and AGE formation with greater effects elicited by MG. Both high glucose and MG-AGE significantly facilitated apoptosis with a more predominant effect from MG-AGE. In addition, phosphorylation of MAPK cascade [extracellular signal-regulated kinase-1/2 (ERK1/2) and p38] and nuclear O-GlcNAcylation were enhanced in MG-AGE-treated myocytes, similar to those elicited by high glucose. MG-AGE-induced phosphorylation of ERK1/2 and p38 was nullified by neutralizing AGE with specific anti-AGE antibody but not nonspecific antiserum. Collectively, these results indicated that AGE or its precursor MG may trigger ROS generation, apoptosis, MAPK activation and nuclear O-GlcNAcylation in human cardiac myocytes, in a manner reminiscent of high extracellular glucose.

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  • A 12-wk high-fat diet in rats induced obesity and elevated serum AGE levels which correlated with increased O-Glc-NAc modifications and apoptosis in cardiomyocytes, similar to apoptosis induced by hyperglycemia.

    “Ren’s group recently demonstrated that a 12-wk high-fat diet in rats induced obesity and elevated serum AGE levels which correlated with increased O-Glc-NAc modifications and apoptosis in cardiomyocytes (205) in a similar manner to the apoptosis induced by hyperglycemia (206).”

    From Cardiac remodeling in obesity (2008) · cites this paper as [206]

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Authors
Li, S.-Y., Sigmon, V. K., Babcock, S. A., & Ren, J.
Affiliations
University of Wyoming (US)
Corresponding author
Ren, Jun
ORCID
Ren, Jun
Venue
Life Sciences
Publisher
Elsevier BV
Published
2007-02
Volume
80
Issue
11
Pages
1051-1056
ISSN
0024-3205 (ISSN-L)
DOI
10.1016/j.lfs.2006.11.035
OpenAlex
W2130695446
Cited by
97
References
21
Citations by year
2026: 1 · 2025: 2 · 2024: 1 · 2023: 3 · 2022: 6 · 2021: 4 · 2020: 2 · 2019: 2 · 2018: 3 · 2017: 15 · 2016: 6 · 2015: 6 · 2014: 3 · 2013: 10 · 2012: 9
FWCI
3.19
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Life Sciences (publishedVersion)
  • PubMed (publishedVersion)
Funders
University of Wyoming
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Glycosylation and Glycoproteins Research
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Keywords
advanced glycation end products, methylglyoxal, reactive oxygen species, apoptosis, MAPK signaling, ERK1/2, p38 MAPK, cardiomyocytes, high glucose, diabetic cardiomyopathy, caspase-3
MeSH terms
Acylation, Animals, Cattle, Cell Nucleus, Cells, Cultured, Fetus, Glucose, Glycosylation, Humans, Pyruvaldehyde, Serum Albumin, Bovine, Glycation End Products, Advanced, Apoptosis, N-Acetylglucosaminyltransferases, Reactive Oxygen Species, Mitogen-Activated Protein Kinase Kinases, Myocytes, Cardiac, Caspase 3, DNA Fragmentation

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