Anti-CA2 polyclonal antibody

Objective: Previous study has shown that Kv4.3, a main coding subunit generating cardiac transient-outward K+ current (Ito), can inhibit Ca2+/calmodulin-dependent protein kinase II (CaMKII) activity. Based on these observations, we speculate that over-expression of Kv4.3 gene could reverse not only Ito reduction but also cardiac remodeling in the rat myocardial infarction (MI) model. Methods and results: Healthy male Sprague-Dawley (SD) rats were used to establish MI model by ligation of left anterior descending coronary artery, and adenovirus integrated with Kv4.3 gene (AD-Kv4.3) was delivered in infarct border zone by intramyocardial injection. The hearts were harvested for histological analysis (HE or Masson trichrome staining), western blot or patch clamp 4 weeks after MI. Our data showed that the application of AD-Kv4.3 could reduce myocardial infarct size and fibrosis, and its cardioprotective effects were similar with medicine therapy (combination of metoprolol and captopril). Moreover, Kv4.3 over-expression significantly improved MI-induced cardiac dysfunction and enhanced Ito density while decreasing corrected QT (QTc) intervals and cardiac electrophysiological instability. Western blot showed that Kv4.3 transfection reduced CaMKII, PLB-17 and ryanodine receptor2 (RyR2 Ser2814) phosphorylation level, at same time increased SERCA2 expression dramatically. Conclusion: Over-expression of Kv4.3 can not only attenuate cardiac electrophysiological instability and cardiac performance, but also reduce myocardial infarct area and cardiac fibrosis. Like traditional anti-remodeling therapy-angiotensin converting enzyme inhibitor (ACEI) combined with beta-adrenergic receptor blocker, overexpression of Kv4.3 seems to be an effective and safe therapy for both structural and electrical remodeling induced by MI via CaMKII inhibition.

Upon herbivore attack, plants emit herbivore-induced plant volatiles (HIPVs). HIPVs can prime defences and resistance of intact plants. However, how HIPVs are decoded and translated into functional defence responses is not well understood, especially in long-lived woody plants. Here, we investigated the impact of the aromatic HIPV indole on defence-related early signalling, phytohormone accumulation, secondary metabolite biosynthesis and herbivore resistance in tea plants. We find that tea plants infested with tea geometrid caterpillars release indole at concentrations >450 ng*hr(-1). Exposure to corresponding doses of synthetic indole primes the expression of early defence genes involved in calcium (Ca2+) signalling, MPK signalling and jasmonate biosynthesis. Indole exposure also primes the production of jasmonates and defence-related secondary metabolites. These changes are associated with higher herbivore resistance of indole-exposed tea plants. Chemical inhibition of Ca2+ and jasmonate signalling provides evidence that both are required for indole-mediated defence priming and herbivore resistance. Our systematic assessment of the impact of indole on defence signalling and deployment shows that indole acts by boosting Ca2+ signalling, resulting in enhanced jasmonate-dependent defence and resistance in a woody plant. Our work extends the molecular basis of HIPV-induced defence priming from annual plants to an economically important tree species.