Cyclin D3/CDK11 p58 Complex Involved in Schwann Cells Proliferation Repression Caused by Lipopolysaccharide
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Cyclin D3/CDK11p58 Complex Involved in Schwann Cells Proliferation Repression Caused by Lipopolysaccharide Yinong Duan,1 Xingxin He,1 Huiguang Yang,2 Yuhong Ji,2 Tao Tao,2 Jinling Chen,1 Ling Hu,2 Fupeng Zhang,2 Xiaohong Li,2 Huimin Wang,1,4 Aiguo Shen,2,4 and Xiang Lu3,4
Abstract—Schwann cells proliferation is the main characterize of kinds PNS inflammation diseases. It has been well documented that cyclin D3 /CDK11p58 complex inhibits cell function through multiple mechanisms, but the mechanism of cyclin D3/CDK11p58 complex exerts its repressive role in the Schwann cells proliferation remains to be identified. In the present investigation, we demonstrated that the expression of CDK11p58 were upregulated in the inflammation caused by LPS, a main part of bactria. Cyclin D3 and the 58-kDa isoform of cyclin-dependent kinase 11 (CDK11p58) interacted with each other mainly in nuclear region, repressed Schwann cells proliferation and induced cell apoptosis. Overexpression of CDK11p58 expression might enhance this process, while silence of cyclin D3 reverting it. This work demonstrates for the first time the role of cyclin D3/CDK11p58 complex in repressing the Schwann cells proliferation and inducing its apoptosis. KEY WORDS: CDK11p58; Cyclin D3; proliferation; apoptosis; Schwann cells; lipopolysaccharide.
cellular and molecular changes in the nerve segment distal to the injury site termed “Wallerian degeneration”. Schwann cells proliferation during Wallerian degeneration results in a marked increase in Schwann cell number in the distal stump [4]. In the schwann cells proliferation, may mechanisms have been invested, including the role of cyclin and the cyclin-dependent kinases (CDK1 through CDK11), but the prccise mechanisms in regulating the proliferation of Schwann cells are still not clarified [5–13]. The PITSLRE protein kinases, and is known as CDK11, are parts of the large family of p34cdc2-related kinases, whose functions appear to be linked with cellcycle control, apoptosis, neuronal physiology, differentiation and transcription [14–16]. The larger CDK11p110 isoforms are associated with cyclin L and various splicing factors, and are involved in the regulation of transcription and RNA splicing in proliferating cells [17–19]. The smaller CDK11p58 isoforms result from translation initiation at an internal ribosome entry site in the CDK11p110 mRNA, and play an important role in mitosis [14, 20]. Recent studies also revealed that CDK11 p 5 8 promotes centrosome
INTRODUCTION Schwann cells proliferation is crucial for the peripheral nervous system (PNS) development, degeneration and regeneration after injury, and tumorigenesis [1–3]. Injury in PNS initiates a sequence of degenerative
Yinong Duan and Xingxin He contributed equally to this work. 1
Laboratory Center, Affiliated Hospital of Nantong University, and Department of Parasitology and Microbiology, Medical College, Nantong University, 19 Qixiu Road, Nantong 226001, People’s Republic of China 2 Department of Immunology, Medical College, Nantong University, Nantong 226
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