GSE211134
Dual-omics reveals the different roles of a1 and ß-adrenergic receptors in acute sympathetic stress-induced cardiac inflammation
Sympathetic overactivation under strong acute stresses triggers acute cardiovascular events including myocardial infarction (MI), sudden cardiac death, and stress cardiomyopathy. a1-ARs and ß-ARs, two dominant subtypes of adrenergic receptors in the heart, play a significant role in the physiological and pathologic regulation of these processes. However, little is known about the functional similarities and differences between a1- and ß-ARs activated temporal responses in stress-induced cardiac pathology. In this work, we systematically compared the cardiac temporal genome-wide profiles of acute a1-AR and ß-AR activation in the mice model by integrating transcriptome and proteome. We found that a1- and ß-AR activations induced sustained and transient inflammatory gene expression, respectively. Particularly, the overactivation of a1-AR but not ß-AR led to neutrophil infiltration at 1 day, which was closely associated with the up-regulation of chemokines, activation of NF-?B pathway, and sustained inflammatory response. Furthermore, there are more metabolic disorders under a1-AR overactivation compared with ß-AR overactivation. These findings provide a new therapeutic strategy that besides using ß-blocker as soon as possible, blocking a1-AR within one day should also be considered in the treatment of acute stress associated cardiovascular diseases. Overall design: RNA-seq of Mouse heart tissue under a1- and ß-AR overactivations.