Upregulation of PLZF is Associated with Neuronal Injury in Lipopolysaccharide-Induced Neuroinflammation

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• 作者：Mingqing He ; Yonghua Liu ; Jiabing Shen ; Chengwei Duan ; Xiang Lu
• 关键词：Lipopolysaccharide ; Neuroinflammation ; PLZF ; Neuronal apoptosis ; Rats
• 刊名：Neurochemical Research
• 出版年：2016
• 出版时间：November 2016
• 年：2016
• 卷：41
• 期：11
• 页码：3063-3073
• 全文大小：1,720 KB
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Neurosciences
  Biochemistry
  Neurology
  
• 出版者：Springer Netherlands
• ISSN：1573-6903
• 卷排序：41

文摘

Promyelocytic leukemia zinc finger (PLZF) protein has been identified as a tumor suppressor in a variety of cancers, including leukemia, malignant mesothelioma, malignant melanoma, pancreatic cancer and prostate cancer. Studies have demonstrated that altered expression of PLZF affected its biological functions associated with tumorigenesis, such as proliferation, cell cycle, and apoptosis. However, information regarding its regulation and possible function in the central nervous system diseases is still limited. In this study, we performed a neuroinflammatory model by lipopolysaccharide (LPS) lateral ventricle injection in adult rats and detected increased expression of PLZF in the brain cortex. Immunofluorescence assay indicated that PLZF was significantly increased in neurons 3 day after LPS injection, but not in astrocytes and microglia. Moreover, there was a concomitant upregulation of active caspase-3, cyclin D1, and CDK4 in vivo and vitro studies. In addition, the expression of these proteins in cortical primary neurons was inhibited after knocking down PLZF by siRNA. Collectively, all these results suggested that the upregulation of PLZF might be involved in neuronal apoptotic-like injury in neuroinflammation after LPS injection.