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Article: Vitamin D Promotes Remyelination by Suppressing c-Myc and Inducing Oligodendrocyte Precursor Cell Differentiation after Traumatic Spinal Cord Injury

TitleVitamin D Promotes Remyelination by Suppressing c-Myc and Inducing Oligodendrocyte Precursor Cell Differentiation after Traumatic Spinal Cord Injury
Authors
KeywordsDifferentiation
Myelination
Oligodendrocyte
Spinal cord injury
Vitamin D
Issue Date2022
Citation
International Journal of Biological Sciences, 2022, v. 18, n. 14, p. 5391-5404 How to Cite?
AbstractDemyelination due to oligodendrocytes loss occurs after traumatic spinal cord injury (TSCI). Several studies have suggested the therapeutic potential of vitamin D (VitD) in demyelinating diseases. However, experimental evidence in the context of TSCI is limited, particularly in the presence of prior VitD-deficiency. In the present study, a contusion and a transection TSCI rat model were used, representing mild and severe injury, respectively. Motor recovery was assessed in rats with normal VitD level or with VitD-deficiency after 8 weeks’ treatment post-TSCI (Cholecalciferol, 500 IU/kg/day). The impact on myelin integrity was examined by transmission electron microscopy and studied in vitro using primary culture of oligodendrocytes. We found that VitD treatment post-TSCI effectively improved hindlimb movement in rats with normal VitD level irrespective of injury severity. However, cord-transected rats with prior deficiency did not seem to benefit from VitD supplementation. Our data further suggested that having sufficient VitD was essential for persevering myelin integrity after injury. VitD rescued oligodendrocytes from apoptotic cell death in vitro and enhanced their myelinating ability towards dorsal root axons. Enhanced myelination was mediated by increased oligodendrocyte precursor cells (OPCs) differentiation into oligodendrocytes in concert with c-Myc downregulation and suppressed OPCs proliferation. Our study provides novel insights into the functioning of VitD as a regulator of OPCs differentiation as well as strong preclinical evidence supporting future clinical testing of VitD for TSCI.
Persistent Identifierhttp://hdl.handle.net/10722/330845
ISSN
2023 Impact Factor: 8.2
2023 SCImago Journal Rankings: 2.114
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLi, Ning-
dc.contributor.authorYao, Min-
dc.contributor.authorLiu, Jiaxin-
dc.contributor.authorZhu, Zhiyuan-
dc.contributor.authorLam, Tsz Lung-
dc.contributor.authorZhang, Pingde-
dc.contributor.authorKiang, Karrie Mei Yee-
dc.contributor.authorLeung, Gilberto Ka Kit-
dc.date.accessioned2023-09-05T12:15:09Z-
dc.date.available2023-09-05T12:15:09Z-
dc.date.issued2022-
dc.identifier.citationInternational Journal of Biological Sciences, 2022, v. 18, n. 14, p. 5391-5404-
dc.identifier.issn1449-2288-
dc.identifier.urihttp://hdl.handle.net/10722/330845-
dc.description.abstractDemyelination due to oligodendrocytes loss occurs after traumatic spinal cord injury (TSCI). Several studies have suggested the therapeutic potential of vitamin D (VitD) in demyelinating diseases. However, experimental evidence in the context of TSCI is limited, particularly in the presence of prior VitD-deficiency. In the present study, a contusion and a transection TSCI rat model were used, representing mild and severe injury, respectively. Motor recovery was assessed in rats with normal VitD level or with VitD-deficiency after 8 weeks’ treatment post-TSCI (Cholecalciferol, 500 IU/kg/day). The impact on myelin integrity was examined by transmission electron microscopy and studied in vitro using primary culture of oligodendrocytes. We found that VitD treatment post-TSCI effectively improved hindlimb movement in rats with normal VitD level irrespective of injury severity. However, cord-transected rats with prior deficiency did not seem to benefit from VitD supplementation. Our data further suggested that having sufficient VitD was essential for persevering myelin integrity after injury. VitD rescued oligodendrocytes from apoptotic cell death in vitro and enhanced their myelinating ability towards dorsal root axons. Enhanced myelination was mediated by increased oligodendrocyte precursor cells (OPCs) differentiation into oligodendrocytes in concert with c-Myc downregulation and suppressed OPCs proliferation. Our study provides novel insights into the functioning of VitD as a regulator of OPCs differentiation as well as strong preclinical evidence supporting future clinical testing of VitD for TSCI.-
dc.languageeng-
dc.relation.ispartofInternational Journal of Biological Sciences-
dc.subjectDifferentiation-
dc.subjectMyelination-
dc.subjectOligodendrocyte-
dc.subjectSpinal cord injury-
dc.subjectVitamin D-
dc.titleVitamin D Promotes Remyelination by Suppressing c-Myc and Inducing Oligodendrocyte Precursor Cell Differentiation after Traumatic Spinal Cord Injury-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.7150/ijbs.73673-
dc.identifier.pmid36147469-
dc.identifier.scopuseid_2-s2.0-85137357124-
dc.identifier.hkuros336447-
dc.identifier.volume18-
dc.identifier.issue14-
dc.identifier.spage5391-
dc.identifier.epage5404-
dc.identifier.isiWOS:000874483300001-

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