S100A11 protects against neuronal cell apoptosis induced by cerebral ischemia via inhibiting the nuclear translocation of annexin A1

• DOI: 10.1038/s41419-018-0686-7
• Publication Date: 2018-05-29T10:21:55Z
• Authors: Qian Xia; Xing Li; Huijuan Zhou; Lu Zheng; Jing Shi
• Keywords: Annexin A1

Abstract The subcellular location of annexin A1 (ANXA1) determines the ultimate fate neurons after ischemic stroke. ANXA1 nuclear translocation is involved in neuronal apoptosis cerebral ischemia, and extracellular also associated with regulation inflammatory responses. As factors mechanism that influence remain unclear, studies aiming to determine clarify role as a cell ‘regulator’ within cells are critically needed. In this study, we found intracerebroventricular injection recombinant adenovirus vector Ad-S100A11 (carrying S100A11) strongly improved cognitive function induced robust neuroprotective effects stroke vivo. Furthermore, upregulation S100A11 protected against by oxygen-glucose deprivation reoxygenation (OGD/R) vitro. Surprisingly, overexpression markedly decreased subsequently alleviated OGD/R-induced apoptosis. Notably, exerted its effect directly binding ANXA1. Importantly, interacted through signal (NTS) ANXA1, which essential for import into nucleus. Consistent our previous studies, OGD/R promoted p53 transcriptional activity, mRNA expression pro-apoptotic Bid gene, activated caspase-3 apoptotic pathway, was almost completely reversed overexpression. Thus, protects inhibiting translocation. This study provides novel whereby apoptosis, suggesting potential previously unidentified treatment strategy minimizing