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Hydrogen sulfide is essential for Schwann cell responses to peripheral nerve injury
Authors:Byung Sun Park  Hyun‐Wook Kim  Im Joo Rhyu  Chan Park  Seung Geun Yeo  Youngbuhm Huh  Na Young Jeong  Junyang Jung
Institution:1. Department of Anatomy and Neurobiology, School of Medicine, Biomedical Science Institution, Kyung Hee University, Seoul, Korea;2. Department of Anatomy, College of Medicine, Korea University, Seoul, Korea;3. Department of Otolaryngology‐Head and Neck Surgery, School of Medicine, Kyung Hee University, Seoul, Korea;4. Department of Anatomy and Cell Biology, College of Medicine, Dong‐A University, Busan, Korea
Abstract:Hydrogen sulfide (H2S) functions as a physiological gas transmitter in both normal and pathophysiological cellular events. H2S is produced from substances by three enzymes: cystathionine β‐synthase (CBS), cystathionine γ‐lyase (CSE), and 3‐mercaptopyruvate sulfurtransferase (MST). In human tissues, these enzymes are involved in tissue‐specific biochemical pathways for H2S production. For example, CBS and cysteine aminotransferase/MST are present in the brain, but CSE is not. Thus, we examined the expression of H2S production‐related enzymes in peripheral nerves. Here, we found that CSE and MST/cysteine aminotransferase, but not CBS, were present in normal peripheral nerves. In addition, injured sciatic nerves in vivo up‐regulated CSE in Schwann cells during Wallerian degeneration (WD); however, CSE was not up‐regulated in peripheral axons. Using an ex vivo sciatic nerve explant culture, we found that the inhibition of H2S production broadly prevented the process of nerve degeneration, including myelin fragmentation, axonal degradation, Schwann cell dedifferentiation, and Schwann cell proliferation in vitro and in vivo. Thus, these results indicate that H2S signaling is essential for Schwann cell responses to peripheral nerve injury.
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Keywords:axonal degradation  cytstathionine‐γ  ‐lyase (CSE)  demyelination  hydrogen sulfide  Schwann cells  Wallerian degeneration
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