title: Upregulation of PLZF is Associated with Neuronal Injury in Lipopolysaccharide-Induced Neuroinflammation.
abstract: 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.
authors.affiliation: Department of Geriatrics, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, 210011, Jiangsu, China.|Department of Geriatrics, The Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
authors.forename: Mingqing
authors.initials: M
authors.lastname: He
authors.affiliation: Department of Pathogen Biology Medical College, Nantong University, Nantong, 226001, Jiangsu, China.
authors.forename: Yonghua
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Department of Neurology, The Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.
authors.forename: Jiabing
authors.initials: J
authors.lastname: Shen
authors.affiliation: The second people's hospital of Nantong, Nantong, 226002, Jiangsu, China.
authors.forename: Chengwei
authors.initials: C
authors.lastname: Duan
authors.affiliation: Department of Geriatrics, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, 210011, Jiangsu, China. luxiang66@njmu.edu.cn.
authors.forename: Xiang
authors.initials: X
authors.lastname: Lu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D002453:Cell Cycle / Q000187:drug effects; D004268:DNA-Binding Proteins / Q000378:metabolism*; D007249:Inflammation / Q000139:chemically induced*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D009474:Neurons / Q000378:metabolism*; D000075722:Promyelocytic Leukemia Zinc Finger Protein; D034741:RNA, Small Interfering / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D015533:Transcriptional Activation / Q000502:physiology; D015854:Up-Regulation
chemical_list: D004268:DNA-Binding Proteins; D008070:Lipopolysaccharides; D000075722:Promyelocytic Leukemia Zinc Finger Protein; D034741:RNA, Small Interfering; C534029:ZBTB16 protein, rat
keywords: Lipopolysaccharide; Neuroinflammation; Neuronal apoptosis; PLZF; Rats