Abstract
BackgroundNeuregulin receptor degradation protein-1 (Nrdp1) is an E3 ubiquitin ligase that plays an important role in regulating cell growth, apoptosis and oxidative stress. However, the data regarding its expression and exact mechanism in neuronal injury following ICH has not been well identified.MethodsIn this study, primary cortical neurons from C57BL/6 mice were subjected to erythrocyte lysates. Nrdp1 expression, cell apoptosis, caspase-3 and BRUCE levels were detected. In addition, inflammatory response, brain edema, and neurological injury in ICH mice were also assessed.ResultsWe found that the expression of Nrdp1 was significantly increased in neuron cells accompanied by up-regulation of active caspase-3 and decreased expression of BRUCE (an inhibitor of apoptosis protein). However, inhibiting Nrdp1 levels of neurons reduced caspase-3 activity but induced up-regulation of BRUCE. In vivo, inhibiting Nrdp1 levels increased pro-inflammatory cytokines, brain edema, and neurological injury following ICH.ConclusionsTaken together, the data suggested that Nrdp1 might play a crucial role in neuronal apoptosis via inhibiting BRUCE following ICH.
Highlights
Neuregulin receptor degradation protein-1 (Nrdp1) is an E3 ubiquitin ligase that plays an important role in regulating cell growth, apoptosis and oxidative stress
Erythrocyte lysates induces Nrdp1 expression in neurons To determine the role of Nrdp1 in response to Intracerebral hemorrhage (ICH), we examined the expression of Nrdp1 expression of neurons after erythrocyte lysates treatment
Nrdp1 promotes neuron apoptosis after erythrocyte lysates treatment To identify whether Nrdp1 contributed to ICH-induced apoptosis in neurons, we transfected neurons with Adcontrol, Ad-Nrdp1 or Ad-si-Nrdp1 before erythrocyte lysates treatment
Summary
Neuregulin receptor degradation protein-1 (Nrdp1) is an E3 ubiquitin ligase that plays an important role in regulating cell growth, apoptosis and oxidative stress. The data regarding its expression and exact mechanism in neuronal injury following ICH has not been well identified. Primary brain injury after ICH leads to hematoma effect and mechanical damage to adjacent brain tissues. Secondary brain injury is a key reason to cause nerve function damage following ICH [4,5,6]. Cell apoptosis is an important factor in secondary brain injury after ICH [4, 7, 8]. Neuregulin receptor degradation protein-1 (Nrdp1), a ring finger E3 ubiquitin ligase, plays an important role in regulating cell growth, apoptosis, oxidative stress and inflammation [12,13,14]
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