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Oligodendrocyte Progenitor Cell Transplantation Ameliorates Preterm Infant Cerebral White Matter Injury in Rats Model

BACKGROUND: Cerebral white matter injury (WMI) is the most common brain injury in preterm infants, leading to motor and developmental deficits often accompanied by cognitive impairment. However, there is no effective treatment. One promising approach for treating preterm WMI is cell replacement ther...

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Autores principales: Wang, Zhaoyan, Zhang, Leping, Yang, Yinxiang, Wang, Qian, Qu, Suqing, Wang, Xiaohua, He, Zhixu, Luan, Zuo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10503552/
https://www.ncbi.nlm.nih.gov/pubmed/37719062
http://dx.doi.org/10.2147/NDT.S414493
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author Wang, Zhaoyan
Zhang, Leping
Yang, Yinxiang
Wang, Qian
Qu, Suqing
Wang, Xiaohua
He, Zhixu
Luan, Zuo
author_facet Wang, Zhaoyan
Zhang, Leping
Yang, Yinxiang
Wang, Qian
Qu, Suqing
Wang, Xiaohua
He, Zhixu
Luan, Zuo
author_sort Wang, Zhaoyan
collection PubMed
description BACKGROUND: Cerebral white matter injury (WMI) is the most common brain injury in preterm infants, leading to motor and developmental deficits often accompanied by cognitive impairment. However, there is no effective treatment. One promising approach for treating preterm WMI is cell replacement therapy, in which lost cells can be replaced by exogenous oligodendrocyte progenitor cells (OPCs). METHODS: This study developed a method to differentiate human neural stem cells (hNSCs) into human OPCs (hOPCs). The preterm WMI animal model was established in rats on postnatal day 3, and OLIG2(+)/NG2(+)/PDGFRα(+)/O4(+) hOPCs were enriched and transplanted into the corpus callosum on postnatal day 10. Then, histological analysis and electron microscopy were used to detect lesion structure; behavioral assays were performed to detect cognitive function. RESULTS: Transplanted hOPCs survived and migrated throughout the major white matter tracts. Morphological differentiation of transplanted hOPCs was observed. Histological analysis revealed structural repair of lesioned areas. Re-myelination of the axons in the corpus callosum was confirmed by electron microscopy. The Morris water maze test revealed cognitive function recovery. CONCLUSION: Our study showed that exogenous hOPCs could differentiate into CC1(+) OLS in the brain of WMI rats, improving their cognitive functions.
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spelling pubmed-105035522023-09-16 Oligodendrocyte Progenitor Cell Transplantation Ameliorates Preterm Infant Cerebral White Matter Injury in Rats Model Wang, Zhaoyan Zhang, Leping Yang, Yinxiang Wang, Qian Qu, Suqing Wang, Xiaohua He, Zhixu Luan, Zuo Neuropsychiatr Dis Treat Original Research BACKGROUND: Cerebral white matter injury (WMI) is the most common brain injury in preterm infants, leading to motor and developmental deficits often accompanied by cognitive impairment. However, there is no effective treatment. One promising approach for treating preterm WMI is cell replacement therapy, in which lost cells can be replaced by exogenous oligodendrocyte progenitor cells (OPCs). METHODS: This study developed a method to differentiate human neural stem cells (hNSCs) into human OPCs (hOPCs). The preterm WMI animal model was established in rats on postnatal day 3, and OLIG2(+)/NG2(+)/PDGFRα(+)/O4(+) hOPCs were enriched and transplanted into the corpus callosum on postnatal day 10. Then, histological analysis and electron microscopy were used to detect lesion structure; behavioral assays were performed to detect cognitive function. RESULTS: Transplanted hOPCs survived and migrated throughout the major white matter tracts. Morphological differentiation of transplanted hOPCs was observed. Histological analysis revealed structural repair of lesioned areas. Re-myelination of the axons in the corpus callosum was confirmed by electron microscopy. The Morris water maze test revealed cognitive function recovery. CONCLUSION: Our study showed that exogenous hOPCs could differentiate into CC1(+) OLS in the brain of WMI rats, improving their cognitive functions. Dove 2023-09-11 /pmc/articles/PMC10503552/ /pubmed/37719062 http://dx.doi.org/10.2147/NDT.S414493 Text en © 2023 Wang et al. https://creativecommons.org/licenses/by-nc/3.0/This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/ (https://creativecommons.org/licenses/by-nc/3.0/) ). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Wang, Zhaoyan
Zhang, Leping
Yang, Yinxiang
Wang, Qian
Qu, Suqing
Wang, Xiaohua
He, Zhixu
Luan, Zuo
Oligodendrocyte Progenitor Cell Transplantation Ameliorates Preterm Infant Cerebral White Matter Injury in Rats Model
title Oligodendrocyte Progenitor Cell Transplantation Ameliorates Preterm Infant Cerebral White Matter Injury in Rats Model
title_full Oligodendrocyte Progenitor Cell Transplantation Ameliorates Preterm Infant Cerebral White Matter Injury in Rats Model
title_fullStr Oligodendrocyte Progenitor Cell Transplantation Ameliorates Preterm Infant Cerebral White Matter Injury in Rats Model
title_full_unstemmed Oligodendrocyte Progenitor Cell Transplantation Ameliorates Preterm Infant Cerebral White Matter Injury in Rats Model
title_short Oligodendrocyte Progenitor Cell Transplantation Ameliorates Preterm Infant Cerebral White Matter Injury in Rats Model
title_sort oligodendrocyte progenitor cell transplantation ameliorates preterm infant cerebral white matter injury in rats model
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10503552/
https://www.ncbi.nlm.nih.gov/pubmed/37719062
http://dx.doi.org/10.2147/NDT.S414493
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