Abstract
LINGO-1 may be involved in the pathogenesis of cerebral ischemia. However, its biological function and underlying molecular mechanism in cerebral ischemia remain to be further defined. In our study, middle cerebral artery occlusion/reperfusion (MACO/R) mice model and HT22 cell oxygen–glucose deprivation/reperfusion (OGD/R) were established to simulate the pathological process of cerebral ischemia in vivo and in vitro and to detect the relevant mechanism. We found that LINGO-1 mRNA and protein were upregulated in mice and cell models. Down-regulation LINGO-1 improved the neurological symptoms and reduced pathological changes and the infarct size of the mice after MACO/R. In addition, LINGO-1 interference alleviated apoptosis and promoted cell proliferation in HT22 of OGD/R. Moreover, down-regulation of LINGO-1 proved to inhibit nuclear translocation of p-NF-κB and reduce the expression level of p-JAK2 and p-STAT3. In conclusion, our data suggest that shLINGO-1 attenuated ischemic injury by negatively regulating NF-KB and JAK2/STAT3 pathways, highlighting a novel therapeutic target for ischemic stroke.
Highlights
Cerebral infarction is a common and frequently occurring disease, with high morbidity, high disability, and high mortality
middle cerebral artery occlusion/reperfusion (MACO/R) mice model and oxygen–glucose deprivation/reperfusion (OGD/R) cell model were established to determine whether LINGO-1 was involved in the brain I/R injury
We found that LINGO-1 was aberrantly up-regulated in the MACO/R model after 1, 7, and 14 days of reperfusion compared to that in the sham group (Fig. 1a)
Summary
Cerebral infarction ( known as a stroke) is a common and frequently occurring disease, with high morbidity, high disability, and high mortality. The side effects of the treatment are to enhance the inflammatory response of the brain capillaries and nerve cell damage after stroke [3, 4]. It is LINGO-1 (leucine-rich repeat- and Ig-containing Nogo receptor-interacting protein-1) is a cell-surface glycoprotein selectively expressed on CNS neurons and oligodendrocytes [5]. A previous study showed that LINGO-1 might be involved in the pathogenesis of cerebral ischemia [6]. We designed this study to determine the effects of LINGO-1 on cerebral I/R injury in vivo ischemic stroke model and in vitro ischemic stroke model
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