Abstract
Inflammation plays a major role in the development of myocardial ischemia-reperfusion (IR) injury. Recombinant human brain natriuretic peptide (rhBNP), a man-made version of a peptide that is elevated in heart failure, exhibits anti-inflammatory effects in various tissues. However, its role in myocardial IR injury remains unclear. In this study, we demonstrate that treatment with rhBNP provided protection for mice against myocardial IR injury as manifested by reduced infarct size and well-preserved myocardial, attenuated inflammatory infiltration and CD4+ T cell proliferation function, and inhibited expression of proinflammatory related genes. Furthermore, mechanistic studies revealed that rhBNP inhibited Jurkat T proliferation by promoting PI3K/AKT/mTOR phosphorylation. Collectively, our data suggest that the administration of rhBNP during IR injury could expand our understanding of the cardioprotective effects of rhBNP.
Highlights
Myocardial ischemia-reperfusion (IR) injury is a major contributor to the morbidity and mortality of coronary artery disease
To gain insight into the mechanisms of Recombinant human brain natriuretic peptide (rhBNP) inhibition of T cell proliferation, we examined the activities of PI3K (p-PI3K), AKT (p-AKT), mTOR (p-mTOR), and P70 S6 kinase (P70S6K) (p-P70S6K) by western blot analysis (Figure 6)
We showed that rhBNP treatment promoted phosphorylation of PI3K, AKT, and mTOR compared with the control group (p < 0:05)
Summary
Myocardial ischemia-reperfusion (IR) injury is a major contributor to the morbidity and mortality of coronary artery disease. IR injury causes progressive necrotic and apoptotic cell death, which compromises cardiac contractility and electrophysiological performance [1]. The main innate immune response to IR injury involves the activation and accumulation of T cells in the postischemic heart [5,6,7]. Depletion of CD4+ T cells in animal models is sufficient to reduce myocardial IR injury [8]. Conventional CD4+ T cells, including Th1 and Th17, play a major role in the development of IR injury [9]. Elimination of T cells by use of lymphocytedeficient RAG1 knockout (KO) mice protected against IR injury [10]. An improved understanding of the underlying molecular mechanisms would be instrumental for the development of CD4+ T cellbased strategies to protect against myocardial IR injury
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
