Neural Regeneration Research ›› 2015, Vol. 10 ›› Issue (10): 1706-1712.doi: 10.4103/1673-5374.167773

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The HMGB1 signaling pathway activates the inflammatory response in Schwann cells

Li-li Man1, #, Fan Liu2, #, Ying-jie Wang1, Hong-hua Song3, Hong-bo Xu4, Zi-wen Zhu1, Qing Zhang1, Yong-jun Wang1,*   

  1. 1 Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu Province, China
    2 Department of Oncology, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China
    3 Department of Pediatrics, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China
    4 Medical College, Nantong University, Nantong, Jiangsu Province, China
  • Received:2015-06-20 Online:2015-10-28 Published:2015-10-28
  • Contact: Yong-jun Wang, Ph.D.,wyjbs@ntu.edu.cn.
  • Supported by:

    This study was supported by the National Natural Science Foundation of China, No. 31471011; a grant from the National Program on Key Basic Research Project of China (973 Program),No. 2014CB542202; the Natural Science Foundation of Jiangsu Province of China, No. BK20131203; a grant from the Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD) of China.

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Abstract:

Schwann cells are not only myelinating cells, but also function as immune cells and express numerous innate pattern recognition receptors, including the Toll-like receptors. Injury to peripheral nerves activates an inflammatory response in Schwann cells. However, it is unclear whether specific endogenous damage-associated molecular pattern molecules are involved in the inflammatory response following nerve injury. In the present study, we demonstrate that a key damage-associated molecular pattern molecule, high mobility group box 1 (HMGB1), is upregulated following rat sciatic nerve axotomy, and we show colocalization of the protein with Schw-ann cells. HMGB1 alone could not enhance expression of Toll-like receptors or the receptor for advanced glycation end products (RAGE), but was able to facilitate migration of Schwann cells. When Schwann cells were treated with HMGB1 together with lipopolysaccharide, the expression levels of Toll-like receptors and RAGE, as well as inflammatory cytokines were upregulated. Our novel findings demonstrate that the HMGB1 pathway activates the inflammatory response in Schwann cells following peripheral nerve injury.

Key words: nerve regeneration, peripheral nerve injury, sciatic nerve transection, Schwann cells, HMGB1, migration, inflammatory response, TLRs, peripheral nerves, DAMPs, cytokines, neural regeneration