Telmisartan cardioprotects from the ischaemic/hypoxic damage through a miR-1-dependent pathway.
Maria Consiglia TrottaBartolo FerraroAntonietta MessinaIacopo PanareseEliana GulottaGiovanni Francesco NicolettiMichele D'AmicoGorizio PierettiPublished in: Journal of cellular and molecular medicine (2019)
The aim of this study was to investigate whether telmisartan protects the heart from the ischaemia/reperfusion damage through a local microRNA-1 modulation. Studies on the myocardial ischaemia/reperfusion injury in vivo and on the cardiomyocyte hypoxia/reoxygenation damage in vitro were done. In vivo, male Sprague-Dawley rats administered for 3 weeks with telmisartan 12 mg/kg/d by gastric gavage underwent ischaemia/reperfusion of the left descending coronary artery. In these rats, infarct size measurement, ELISA, immunohistochemistry (IHC) and reverse transcriptase real-time polymerase chain reaction showed that expressions of connexin 43, potassium voltage-gated channel subfamily Q member 1 and the protein Bcl-2 were significantly increased by telmisartan in the reperfused myocardium, paralleled by microRNA-1 down-regulation. In vitro, the transfection of cardiomyocytes with microRNA-1 reduced the expressions of connexin 43, potassium voltage-gated channel subfamily Q member 1 and Bcl-2 in the cells. Telmisartan (50 µmol/L) 60 minutes before hypoxia/reoxygenation, while not affecting the levels of miR-1 in transfected cells in normoxic condition, almost abolished the increment of miR-1 induced by the hypoxia/reoxygenation to transfected cells. All together, telmisartan cardioprotected against the myocardial damage through the microRNA-1 modulation, and consequent modifications of its downstream target connexin 43, potassium voltage-gated channel subfamily Q member 1 and Bcl-2.
Keyphrases
- induced apoptosis
- oxidative stress
- endoplasmic reticulum stress
- cell proliferation
- acute myocardial infarction
- coronary artery
- cell cycle arrest
- long non coding rna
- signaling pathway
- long noncoding rna
- left ventricular
- cerebral ischemia
- acute ischemic stroke
- atrial fibrillation
- small molecule
- pulmonary hypertension
- subarachnoid hemorrhage
- brain injury
- acute coronary syndrome
- pulmonary arterial hypertension