Schwann-Cell Autophagy, Functional Recovery, and Scar Reduction After Peripheral Nerve Repair

Po Yen Ko, Cheng Chang Yang, Yao Lung Kuo, Fong Chin Su, Tai I. Hsu, Yuan Kun Tu, I. Ming Jou

研究成果: Article同行評審

29 引文 斯高帕斯(Scopus)


The functional outcome after peripheral nerve repair is often unpredictable for many reasons, e.g., the severity of neuronal death and scarring. Axonal degeneration significantly affects outcomes. Post-injury axonal degeneration in peripheral nerves is accompanied by myelin degradation initiated by Schwann cells (SCs), which activate autophagy, a ubiquitous cytoprotective process essential for degrading and recycling cellular constituents. Scar formation occurs concomitantly with nerve insult and axonal degeneration. The association between SC autophagy and the mechanisms of nerve scar formation is still unknown. A rat model of peripheral nerve lesions induced by sciatic nerve transection injuries was used to examine the function of autophagy in fibrosis reduction during the early phase of nerve repair. Rats were treated with rapamycin (autophagy inducer) or 3-methyladenine (autophagy inhibitor). One week after the nerve damage, fibrosis was potently inhibited in rapamycin-treated rats and, based on gait analysis, yielded a better functional outcome. Immunohistochemistry showed that the autophagic activity of SCs and the accumulation of neurofilaments were upregulated in rapamycin-treated rats. A deficiency of SC autophagic activity might be an early event in nerve scar formation, and modulating autophagy might be a powerful pharmacological approach for improving functional outcomes.

頁(從 - 到)601-610
期刊Journal of Molecular Neuroscience
出版狀態Published - 2018 4月 1

All Science Journal Classification (ASJC) codes

  • 細胞與分子神經科學


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