ArticleThe Journal of biological chemistry2014
Regulation of large conductance Ca2+-activated K+ (BK) channel β1 subunit expression by muscle RING finger protein 1 in diabetic vessels.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Impact of Sorbs2 dysfunction on cardiovascular diseases.Biochimica et biophysica acta. Molecular basis of disease · 2025Review
- A new mechanism of high-altitude adaptation reducing myocardium infarction: inhibiting inflammation-induced ubiquitin degradation of BKBasic research in cardiology · 2025Article
- Sorbs2 Deficiency and Vascular BK Channelopathy in Diabetes.Circulation research · 2024Article
- CaInternational journal of molecular sciences · 2023Review
- Large-conductance CaFrontiers in cardiovascular medicine · 2022Article
- Coronary Large Conductance CaFrontiers in physiology · 2021Review
- Knockout of AKAP150 improves impaired BK channel-mediated vascular dysfunction through the Akt/GSK3β signalling pathway in diabetes mellitus.Journal of cellular and molecular medicine · 2020Article
- Regulation of KCNMA1 transcription by Nrf2 in coronary arterial smooth muscle cells.Journal of molecular and cellular cardiology · 2020Article
- BK Channel Dysfunction in Diabetic Coronary Artery: Role of the E3 Ubiquitin Ligases.Frontiers in physiology · 2020Review
- F-box protein-32 down-regulates small-conductance calcium-activated potassium channel 2 in diabetic mouse atria.The Journal of biological chemistry · 2019Article
- Downregulation of BK channel function and protein expression in coronary arteriolar smooth muscle cells of type 2 diabetic patients.Cardiovascular research · 2019Article
- Diabetes Mellitus and Ischemic Heart Disease: The Role of Ion Channels.International journal of molecular sciences · 2018Review
- Mechanisms of BK Channel Activation by Docosahexaenoic Acid in Rat Coronary Arterial Smooth Muscle Cells.Frontiers in pharmacology · 2018Article
- CRL4 antagonizes SCFFbxo7-mediated turnover of cereblon and BK channel to regulate learning and memory.PLoS genetics · 2018Article
- Role of the endothelial caveolae microdomain in shear stress-mediated coronary vasorelaxation.The Journal of biological chemistry · 2017Article
- Article
- Association between potassium channel SNPs and essential hypertension in Xinjiang Kazak Chinese patients.Experimental and therapeutic medicine · 2017Article
- Pregnancy Reprograms Large-Conductance CaHypertension (Dallas, Tex. : 1979) · 2017Article
- Differential distribution and functional impact of BK channel beta1 subunits across mesenteric, coronary, and different cerebral arteries of the rat.Pflugers Archiv : European journal of physiology · 2017Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The large conductance Ca(2+)-activated K(+) (BK) channel, expressed abundantly in vascular smooth muscle cells (SMCs), is a key determinant of vascular tone. BK channel activity is tightly regulated by its accessory β1 subunit (BK-β1). However, BK channel function is impaired in diabetic vessels by increased ubiquitin/proteasome-dependent BK-β1 protein degradation. Muscle RING finger protein 1 (MuRF1), a muscle-specific ubiquitin ligase, is implicated in many cardiac and skeletal muscle diseases. However, the role of MuRF1 in the regulation of vascular BK channel and coronary function has not been examined. In this study, we hypothesized that MuRF1 participated in BK-β1 proteolysis, leading to the down-regulation of BK channel activation and impaired coronary function in diabetes. Combining patch clamp and molecular biological approaches, we found that MuRF1 expression was enhanced, accompanied by reduced BK-β1 expression, in high glucose-cultured human coronary SMCs and in diabetic vessels. Knockdown of MuRF1 by siRNA in cultured human SMCs attenuated BK-β1 ubiquitination and increased BK-β1 expression, whereas adenoviral expression of MuRF1 in mouse coronary arteries reduced BK-β1 expression and diminished BK channel-mediated vasodilation. Physical interaction between the N terminus of BK-β1 and the coiled-coil domain of MuRF1 was demonstrated by pulldown assay. Moreover, MuRF1 expression was regulated by NF-κB. Most importantly, pharmacological inhibition of proteasome and NF-κB activities preserved BK-β1 expression and BK-channel-mediated coronary vasodilation in diabetic mice. Hence, our results provide the first evidence that the up-regulation of NF-κB-dependent MuRF1 expression is a novel mechanism that leads to BK channelopathy and vasculopathy in diabetes.
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