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Published on: May 3, 2024
Cyclin D3/CDK11(p58) complex involved in Schwann cells proliferation repression caused by lipopolysaccharide
Yinong Duan1, Xingxin He, Huiguang Yang
1Laboratory Center, Affiliated Hospital of Nantong University, and Department of Parasitology and Microbiology, Medical College, Nantong University, 19 Qixiu Road, Nantong, People's Republic of China.
Abstract:
Schwann cells proliferation is the main characterize of kinds PNS inflammation diseases. It has been well documented that cyclin D3 /CDK11(p58) complex inhibits cell function through multiple mechanisms, but the mechanism of cyclin D3/CDK11(p58) complex exerts its repressive role in the Schwann cells proliferation remains to be identified. In the present investigation, we demonstrated that the expression of CDK11(p58) were upregulated in the inflammation caused by LPS, a main part of bacteria. Cyclin D3 and the 58-kDa isoform of cyclin-dependent kinase 11 (CDK11(p58)) interacted with each other mainly in nuclear region, repressed Schwann cells proliferation and induced cell apoptosis. Overexpression of CDK11(p58) expression might enhance this process, while silence of cyclin D3 reverting it. This work demonstrates for the first time the role of cyclin D3/CDK11(p58) complex in repressing the Schwann cells proliferation and inducing its apoptosis.
Insights
The cyclin D3/CDK11(p58) complex suppresses Schwann cell proliferation and promotes apoptosis in peripheral nervous system inflammation. This study reveals the complex
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Background:
- Schwann cell proliferation is a hallmark of peripheral nervous system (PNS) inflammatory diseases.
- The cyclin D3/CDK11(p58) complex is known to inhibit cell functions via various mechanisms.
- The specific role of cyclin D3/CDK11(p58) in regulating Schwann cell proliferation requires elucidation.
Purpose of the Study:
- To investigate the mechanism by which the cyclin D3/CDK11(p58) complex represses Schwann cell proliferation.
- To determine the role of cyclin D3/CDK11(p58) in PNS inflammation.
Main Methods:
- Examined CDK11(p58) expression in LPS-induced inflammation.
- Assessed the interaction between cyclin D3 and CDK11(p58) using cell biology techniques.
- Investigated the effects of CDK11(p58) overexpression and cyclin D3 silencing on Schwann cell proliferation and apoptosis.
Main Results:
- CDK11(p58) expression was upregulated in LPS-induced inflammation.
- Cyclin D3 and CDK11(p58) interacted within the nucleus, inhibiting Schwann cell proliferation and inducing apoptosis.
- Overexpression of CDK11(p58) enhanced these effects, while silencing cyclin D3 reversed them.
Conclusions:
- The cyclin D3/CDK11(p58) complex plays a crucial role in repressing Schwann cell proliferation.
- This complex also induces apoptosis in Schwann cells during PNS inflammation.
- This study provides the first evidence for the function of the cyclin D3/CDK11(p58) complex in Schwann cell regulation.
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