ArticleCardiovascular drugs and therapy2015
Valsartan Upregulates Kir2.1 in Rats Suffering from Myocardial Infarction via Casein Kinase 2.
Article in Cardiovascular drugs and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Immunomodulatory Effects of RAAS Inhibitors: Beyond Hypertension and Heart Failure.Biomedicines · 2025Review
- Role of post-translational modifications of Sp1 in cardiovascular diseases.Frontiers in cell and developmental biology · 2024Review
- Angiotensin Regulation of Vascular Homeostasis: Exploring the Role of ROS and RAS Blockers.International journal of molecular sciences · 2023Review
- Tetramisole is a new IPharmacology research & perspectives · 2022Review
- Glycogen synthase kinase 3 beta inhibitor SB216763 improves Kir2.1 expression after myocardia infraction in rats.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2022Article
- Gentiopicroside Ameliorates Diabetic Renal Tubulointerstitial FibrosisFrontiers in pharmacology · 2022Article
- Protein kinase CK2 and ion channels (Review).Biomedical reports · 2020Review
- Towards the Development of AgoKirs: New Pharmacological Activators to Study KInternational journal of molecular sciences · 2020Review
- Modulation of transcriptional mineralocorticoid receptor activity by casein kinase 2.Scientific reports · 2017Article
- Soluble epoxide hydrolase inhibitors, t-AUCB, regulated microRNA-1 and its target genes in myocardial infarction mice.Oncotarget · 2017Article
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10 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
purposeMyocardial infarction (MI) results in an increased susceptibility to ventricular arrhythmias, due in part to decreased inward-rectifier K+ current (IK1), which is mediated primarily by the Kir2.1 protein. The use of renin-angiotensin-aldosterone system antagonists is associated with a reduced incidence of ventricular arrhythmias. Casein kinase 2 (CK2) binds and phosphorylates SP1, a transcription factor of KCNJ2 that encodes Kir2.1. Whether valsartan represses CK2 activation to ameliorate IK1 remodeling following MI remains unclear.
methodsWistar rats suffering from MI received either valsartan or saline for 7 days. The protein levels of CK2 and Kir2.1 were each detected via a Western blot analysis. The mRNA levels of CK2 and Kir2.1 were each examined via quantitative real-time PCR.
resultsCK2 expression was higher at the infarct border; and was accompanied by a depressed IK1/Kir2.1 protein level. Additionally, CK2 overexpression suppressed KCNJ2/Kir2.1 expression. By contrast, CK2 inhibition enhanced KCNJ2/Kir2.1 expression, establishing that CK2 regulates KCNJ2 expression. Among the rats suffering from MI, valsartan reduced CK2 expression and increased Kir2.1 expression compared with the rats that received saline treatment. In vitro, hypoxia increased CK2 expression and valsartan inhibited CK2 expression. The over-expression of CK2 in cells treated with valsartan abrogated its beneficial effect on KCNJ2/Kir2.1.
conclusionsAT1 receptor antagonist valsartan reduces CK2 activation, increases Kir2.1 expression and thereby ameliorates IK1 remodeling after MI in the rat model.
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