Bud endodormancy represents a pivotal and intricate biological process influenced by both genetic and epigenetic factors, the exact mechanism of which remains elusive. Hydrogen peroxide (H2O2) functions as a signallin...
详细信息
Bud endodormancy represents a pivotal and intricate biological process influenced by both genetic and epigenetic factors, the exact mechanism of which remains elusive. Hydrogen peroxide (H2O2) functions as a signalling molecule in the regulation of dormancy, with peroxidase (POD) playing a crucial role in governing H2O2 levels. Our prior transcriptomic and metabolomic investigations into diverse pear dormancy phases posited that POD predominantly oversees pear bud dormancy. In this study, we utilised qRT-PCR to screen the most significantly expressed gene, Pyrus pyrifolia POD4-like (PpPOD4-like), from seven POD genes. Subsequently, H2O2 test kits, overexpression methods, and subcellular localisation techniques were employed to assess changes in H2O2 content, POD activity, PpPOD4-like expression, and its cellular positioning during pear bud dormancy. Subcellular localisation experiments revealed that PpPOD4-like is situated on the cell membranes. Notably, H2O2 content exhibited a rapid increase during endodormancy and decreased swiftly after ecodormancy. The fluctuation pattern of POD activity aligned with that of H2O2 content. Additionally, PpPOD4-like expression was markedly upregulated, displaying an overall upward trajectory. Our findings indicate that PpPOD4-like modulates H2O2 levels by regulating POD activity, thereby actively participating in the intricate regulation of pear dormancy processes.
Aims: Arrhythmogenesis of chronic myocardial infarction (MI) is associated with the prolongation of action potential, reduction of inward rectifier potassium (I-K1, Kir) channels and hyper-activity of Calcium/calmodul...
详细信息
Aims: Arrhythmogenesis of chronic myocardial infarction (MI) is associated with the prolongation of action potential, reduction of inward rectifier potassium (I-K1, Kir) channels and hyper-activity of Calcium/calmodulin-dependent kinase II (CaMKII) in cardiomyocytes. Zacopride, a selective I-K1 agonist, was applied to clarify the cardioprotection of I-K1 agonism via a CaMKII signaling on arrhythmias post-MI. Methods: Male SD rats were implanted wireless transmitter in the abdominal cavity and subjected to left main coronary artery ligation or sham operation. The telemetric ECGs were monitored per day throughout 4 weeks. At the endpoint, isoproterenol (1.28 mg/kg, i.v.) was administered for provocation test. The expressions of Kir2.1 (dominant subunit of I-K1 in ventricle) and CaMKII were detected by Western-blotting. Key findings: In the telemetric rats post-MI, zacopride significantly reduced the episodes of atrioventricular conduction block (AVB), premature ventricular contraction (PVC), ventricular tachycardia (VT) and ventricular fibrillation (VF), without significant effect on superventricular premature contraction (SPVC). In provocation test, zacopride suppressed the onset of ventricular arrhythmias in conscious PMI or sham rats. The expression of Kir2.1 was significantly downregulated and p-CaMKII was upregulated post-MI, whereas both were restored by zacopride treatment. Significance: I-K1/Kir2.1 might be an attractive target for pharmacological controlling of lethal arrhythmias post MI.
暂无评论