ArticlePloS one2017
Myocardial ischemia-reperfusion enhances transcriptional expression of endothelin-1 and vasoconstrictor ETB receptors via the protein kinase MEK-ERK1/2 signaling pathway in rat.
Article in PloS one, 2017. 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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12 citing papers in PubMed, 29 citations in OpenAlex.
- The Impact of Trimetazidine on Cardiac Fibrosis, Inflammation, and Function in Ischemic Cardiomyopathy Patients.Cardiovascular drugs and therapy · 2023Trial
- Snake Venom Components as Therapeutic Drugs in Ischemic Heart Disease.Biomolecules · 2023Review
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- China Tongxinluo Study for myocardial protection in patients with Acute Myocardial Infarction (CTS-AMI): Rationale and design of a randomized, double-blind, placebo-controlled, multicenter clinical trial.American heart journal · 2020Article
- Heart‑lung crosstalk in pulmonary arterial hypertension following myocardial infarction (Review).International journal of molecular medicine · 2020Review
- MiR-25 exerts cardioprotective effect in a rat model of myocardial ischemia-reperfusion injury by targeting high-mobility group box 1.Journal of the Chinese Medical Association : JCMA · 2020Article
- Unraveling the Mystery of Cold Stress-Induced Myocardial Injury.Frontiers in physiology · 2020Review
- miR-30c-5p Reduces Renal Ischemia-Reperfusion Involving Macrophage.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Biomechanical stress in myocardial infarctions: can endothelin-1 and growth differentiation factor 15 serve as immunohistochemical markers?International journal of legal medicine · 2018Article
- Aerobic exercise combined with huwentoxin-I mitigates chronic cerebral ischemia injury.Neural regeneration research · 2017Article
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Authors and funding
6 authors at 1 institution in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundCoronary artery remodelling and vasospasm is a complication of acute myocardial ischemia and reperfusion. The underlying mechanisms are complex, but the vasoconstrictor peptide endothelin-1 is suggested to have an important role. This study aimed to determine whether the expression of endothelin-1 and its receptors are regulated in the myocardium and in coronary arteries after experimental ischemia-reperfusion. Furthermore, we evaluated whether treatment with a specific MEK1/2 inhibitor, U0126, modified the expression and function of these proteins. METHODS AND
findingsSprague-Dawley rats were randomly divided into three groups: sham-operated, ischemia-reperfusion with vehicle treatment and ischemia-reperfusion with U0126 treatment. Ischemia was induced by ligating the left anterior descending coronary artery for 30 minutes followed by reperfusion. U0126 was administered before ischemia and repeated 6 hours after start of reperfusion. The contractile properties of isolated coronary arteries to endothelin-1 and sarafotoxin 6c were evaluated using wire-myography. The gene expression of endothelin-1 and endothelin receptors were measured using qPCR. Distribution and localization of proteins (pERK1/2, prepro-endothelin-1, endothelin-1, and endothelin ETA and ETB receptors) were analysed by Western blot and immunohistochemistry. We found that pERK1/2 was significantly augmented in the ischemic area 3 hours after ischemia-reperfusion; this correlated with increased ETB receptor and ET-1 gene expressions in ischemic myocardium and in coronary arteries. ETB receptor-mediated vasoconstriction was observed to be increased in coronary arteries 24 hours after ischemia-reperfusion. Treatment with U0126 reduced pERK1/2, expression of ET-1 and ETB receptor, and ETB receptor-mediated vasoconstriction.
conclusionsThese findings suggest that the MEK-ERK1/2 signaling pathway is important for regulating endothelin-1 and ETB receptors in myocardium and coronary arteries after ischemia-reperfusion in the ischemic region. Inhibition of the MEK-ERK1/2 pathway may provide a novel target for reducing ischemia-reperfusion damage in the heart.
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