Key result
Notch1 signaling is activated during ischemic preconditioning and postconditioning, and its activation mediates cardioprotection by reducing infarct size and improving cardiac function.
Why the study?
Does lentiviral overexpression of N1ICD improve cardioprotection (cell viability, infarct size, cardiac function) in rat cardiomyocytes and isolated hearts exposed to ischemia/reperfusion injury?
Does lentiviral overexpression of N1ICD improve cardioprotection (cell viability, infarct size, cardiac function) in rat cardiomyocytes and isolated hearts exposed to ischemia/reperfusion injury?
Notch1 signaling is activated during and mediates the cardioprotective effects of ischemic preconditioning and postconditioning, highlighting it as a potential pharmacological target for ischemic heart disease.
Answers are grounded in this paper and cite their sources.
Notch1 activation may offer a target for cardioprotection in ischemia; animal data leave open clinical translation.
BACKGROUND: Notch signaling is known to be activated following myocardial ischemia, but its role in cardioprotection provided by ischemic preconditioning (IPC) and ischemic postconditioning (IPost) remains unclear. METHODS: Lentiviral vectors were constructed to overexpress or knockdown N1ICD in H9c2 cardiomyocyte and rat heart exposed to ischemia reperfusion injury (IRI), IPC or IPost. RESULTS: Notch1 signaling was activated during myocardial IPC and IPost, and could enhance cell viability and inhibit apoptosis. Furthermore, activated Notch1 signaling stabilized mitochondrial membrane potential and reduced reactive oxygen species induced by IRI. The cardioprotection provided by activated Notch1 signaling resembled that of IPC and IPost, which was related to Stat3 activation and regulation of apoptosis related proteins. Furthermore, in langendorff heart perfusion model, activated Notch1 signaling restored cardiac function, decreased lactate dehydrogenase release and limited infarct size after myocardial ischemia. CONCLUSIONS: Notch1 signaling is activated and mediates cardioprotection provided by IPC and Ipost. Notch1 signaling may represent a potential new pharmacologic mimic for cardioprotection of ischemic heart disease.
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Zhou et al. (2013) studied Myocardial ischemia reperfusion injury. Notch1 signaling activation (N1ICD overexpression) or knockdown vs. Control/Mock vectors and Ischemia/Reperfusion alone was evaluated on Cardioprotection (infarct size, cardiac function, cell viability, apoptosis) (p=<0.05). Notch1 signaling is activated during ischemic preconditioning and postconditioning, and its activation mediates cardioprotection by reducing infarct size and improving cardiac function.
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