ArticleBMC cell biology2011
AGE-BSA down-regulates endothelial connexin43 gap junctions.
Article in BMC cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Identifying and establishing the critical elements of a human cardiac in-vitro model for studying type-II diabetes.Discover applied sciences · 2025Article
- Of cells and tissues: Identifying the elements of a diabetic cardiac in vitro study model.Research square · 2024Article
- Acute Methylglyoxal-Induced Damage in Blood-Brain Barrier and Hippocampal Tissue.Neurotoxicity research · 2022Article
- Article
- Autophagy and Glycative Stress: A Bittersweet Relationship in Neurodegeneration.Frontiers in cell and developmental biology · 2021Review
- Relationships between advanced glycation end products (AGEs), vasoactive substances, and vascular function.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2021Article
- p38 MAPK Pathway in the Heart: New Insights in Health and Disease.International journal of molecular sciences · 2020Review
- Upregulation of connexin43 by glucose deprivation in H9c2 cells via the extracellular signal‑regulated kinase/mitogen‑activated protein kinase signaling pathway.Molecular medicine reports · 2018Article
- Connexin channel and its role in diabetic retinopathy.Progress in retinal and eye research · 2017Review
- Methylglyoxal Induces Changes in the Glyoxalase System and Impairs Glutamate Uptake Activity in Primary Astrocytes.Oxidative medicine and cellular longevity · 2017Article
- Advanced glycation end products impair K(Ca)3.1- and K(Ca)2.3-mediated vasodilatation via oxidative stress in rat mesenteric arteries.Pflugers Archiv : European journal of physiology · 2014Article
- Advanced Glycation End Product (AGE)-AGE Receptor (RAGE) System Upregulated Connexin43 Expression in Rat Cardiomyocytes via PKC and Erk MAPK Pathways.International journal of molecular sciences · 2013Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAdvanced glycation end products generated in the circulation of diabetic patients were reported to affect the function of vascular wall. We examined the effects of advanced glycation end products-bovine serum albumin (AGE-BSA) on endothelial connexin43 (Cx43) expression and gap-junction communication.
resultsIn human aortic endothelial cells (HAEC) treated with a series concentrations of AGE-BSA (0-500 μg/ml) for 24 and 48 hours, Cx43 transcript and Cx43 protein were reduced in a dose dependent manner. In addition, gap-junction communication was reduced. To clarify the mechanisms underlying the down-regulation, MAPKs pathways in HAEC were examined. Both a MEK1 inhibitor (PD98059) and a p38 MAPK inhibitor (SB203580) significantly reversed the reductions of Cx43 mRNA and protein induced by AGE-BSA. Consistently, phosphorylation of ERK and p38 MAPK was enhanced in response to exposure to AGE-BSA. However, all reversions of down-regulated Cx43 by inhibitors did not restore the functional gap-junction communication.
conclusionsAGE-BSA down-regulated Cx43 expression in HAEC, mainly through reduced Cx43 transcription, and the process involved activation of ERK and p38 MAPK.
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