ArticleAmerican journal of physiology. Cell physiology2015
The SUR2B subunit of rat vascular KATP channel is targeted by miR-9a-3p induced by prolonged exposure to methylglyoxal.
Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Potassium channel-targeted therapy in reducing vascular complications in diabetes mellitus: novel insights.Frontiers in pharmacology · 2026Review
- Linking Diabetes Mellitus with Alzheimer's Disease: Bioinformatics Analysis for the Potential Pathways and Characteristic Genes.Biochemical genetics · 2022Article
- Metabolic Shades of S-D-Lactoylglutathione.Antioxidants (Basel, Switzerland) · 2022Review
- miR-450a-5p Eliminates MGO-Induced Insulin Resistance via Targeting CREB.International journal of stem cells · 2020Article
- Mechanisms underlying suppression of noradrenaline-induced contraction by prolonged treatment with advanced glycation end-products in organ-cultured rat carotid artery.Pflugers Archiv : European journal of physiology · 2020Article
- Dicarbonyl Stress and S-Glutathionylation in Cerebrovascular Diseases: A Focus on Cerebral Cavernous Malformations.Antioxidants (Basel, Switzerland) · 2020Review
- Review
- miR-214-Dependent Increase of PHLPP2 Levels Mediates the Impairment of Insulin-Stimulated Akt Activation in Mouse Aortic Endothelial Cells Exposed to Methylglyoxal.International journal of molecular sciences · 2018Article
- Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Methylglyoxal-Glyoxalase 1 Balance: The Root of Vascular Damage.International journal of molecular sciences · 2017Review
- Overexcited MaxiK and KScientific reports · 2016Article
- RNA Regulation of Lipotoxicity and Metabolic Stress.Diabetes · 2016Review
- Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders.Pharmacological reviews · 2016Review
- Diagnostic, Prognostic, and Therapeutic Value of Circulating miRNAs in Heart Failure Patients Associated with Oxidative Stress.Oxidative medicine and cellular longevity · 2016Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
ATP-sensitive K(+) (K(ATP)) channels regulate plasma membrane excitability. The Kir6.1/SUR2B isoform of K(ATP) channels is expressed in vascular smooth muscles and plays an important role in vascular tone regulation. This K(ATP) channel is targeted by several reactive species. One of them is methylglyoxal (MGO), which is overly produced with persistent hyperglycemia and contributes to diabetic vascular complications. We have previously found that MGO causes posttranscriptional inhibition of the K(ATP) channel, aggravating vascular tone regulation. Here we show evidence for the underlying molecular mechanisms. We screened microRNA databases and found several candidates. Of them, miR-9a-3p, increased its expression level by ∼240% when the cultured smooth muscle cell line was exposed to micromolar concentrations of MGO. Treatments with exogenous miR-9a-3p downregulated the SUR2B but not Kir6.1 mRNA. Antisense nucleotides of miR-9a-3p alleviated the effects of MGO. Quantitative PCR showed that the targeting sites of the miR-9a-3p were likely to be in the coding region of SUR2B. The effects of miR-9a-3p were mostly eliminated when the potential targeting site in SUR2B was site-specifically mutated. Our functional assays showed that K(ATP) currents were impaired by miR-9a-3p induced with MGO treatment. These results suggest that MGO exposure raises the expression of miR-9a-3p, which subsequently downregulates the SUR2B mRNA, compromising K(ATP) channel function in vascular smooth muscle.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.