Human iPSC-derived spinal neural progenitors enhance sensorimotor recovery in spinal cord-injured NOD-SCID mice via differentiation and microenvironment regulation

Abstract Spinal cord injury (SCI) remains a significant clinical challenge and poses a dramatic threat to the life quality of patients due to limited neural regeneration and detrimental post-injury alternations in tissue microenvironment. We developed a therapeutic approach by transplanting spinal n...

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Main Authors: Xuanbao Yao, Kehua Zhang, Tao Na, Yuchun Wang, Yuhan Guo, Jiajie Xi, Xiang Li, Shufang Meng, Miao Xu
Format: Article
Language:English
Published: Nature Publishing Group 2025-08-01
Series:Cell Death and Disease
Online Access:https://doi.org/10.1038/s41419-025-07961-x
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author Xuanbao Yao
Kehua Zhang
Tao Na
Yuchun Wang
Yuhan Guo
Jiajie Xi
Xiang Li
Shufang Meng
Miao Xu
author_facet Xuanbao Yao
Kehua Zhang
Tao Na
Yuchun Wang
Yuhan Guo
Jiajie Xi
Xiang Li
Shufang Meng
Miao Xu
author_sort Xuanbao Yao
collection DOAJ
description Abstract Spinal cord injury (SCI) remains a significant clinical challenge and poses a dramatic threat to the life quality of patients due to limited neural regeneration and detrimental post-injury alternations in tissue microenvironment. We developed a therapeutic approach by transplanting spinal neural progenitor cells (spNPGs), derived from human induced pluripotent stem cell (iPSC)-generated neuromesodermal progenitors, into a contusive SCI model in NOD-SCID mice. Single-cell RNA sequencing mapped the in vitro differentiation of iPSC-spNPGs, confirming their specification into spinal neuronal lineages. Single-nucleus transcriptomics at 1 week post-transplantation showed that the grafted cells differentiated in vivo into motor neurons and two interneuron subtypes (V2 and dI4). Additionally, spNPGs integrated into host neural circuits, enhancing synaptic connectivity, while simultaneously modulating the injury microenvironment by shifting microglia and astrocyte polarization toward anti-inflammatory and neuroprotective phenotypes. This dual mechanism promoted axonal regrowth, remyelination, and significant sensorimotor recovery, as evidenced by improved locomotor scores. Our findings highlight the therapeutic potential of human iPSC-spNPGs in reconstructing neural networks and mitigating secondary damage, providing compelling preclinical evidence for advancing stem cell-based SCI therapies.
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institution Kabale University
issn 2041-4889
language English
publishDate 2025-08-01
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series Cell Death and Disease
spelling doaj-art-c4d4e9fa6b1e417f98fe178689a41e9c2025-08-24T11:54:31ZengNature Publishing GroupCell Death and Disease2041-48892025-08-0116111410.1038/s41419-025-07961-xHuman iPSC-derived spinal neural progenitors enhance sensorimotor recovery in spinal cord-injured NOD-SCID mice via differentiation and microenvironment regulationXuanbao Yao0Kehua Zhang1Tao Na2Yuchun Wang3Yuhan Guo4Jiajie Xi5Xiang Li6Shufang Meng7Miao Xu8Graduate School of Guangzhou Medical University, Guangzhou Medical UniversityNational Institutes for Food and Drug ControlNational Institutes for Food and Drug ControlNational Institutes for Food and Drug ControlNational Institutes for Food and Drug ControlXellSmart Biomedical (Suzhou) Co., LtdXellSmart Biomedical (Suzhou) Co., LtdNational Institutes for Food and Drug ControlGuangzhou National LaboratoryAbstract Spinal cord injury (SCI) remains a significant clinical challenge and poses a dramatic threat to the life quality of patients due to limited neural regeneration and detrimental post-injury alternations in tissue microenvironment. We developed a therapeutic approach by transplanting spinal neural progenitor cells (spNPGs), derived from human induced pluripotent stem cell (iPSC)-generated neuromesodermal progenitors, into a contusive SCI model in NOD-SCID mice. Single-cell RNA sequencing mapped the in vitro differentiation of iPSC-spNPGs, confirming their specification into spinal neuronal lineages. Single-nucleus transcriptomics at 1 week post-transplantation showed that the grafted cells differentiated in vivo into motor neurons and two interneuron subtypes (V2 and dI4). Additionally, spNPGs integrated into host neural circuits, enhancing synaptic connectivity, while simultaneously modulating the injury microenvironment by shifting microglia and astrocyte polarization toward anti-inflammatory and neuroprotective phenotypes. This dual mechanism promoted axonal regrowth, remyelination, and significant sensorimotor recovery, as evidenced by improved locomotor scores. Our findings highlight the therapeutic potential of human iPSC-spNPGs in reconstructing neural networks and mitigating secondary damage, providing compelling preclinical evidence for advancing stem cell-based SCI therapies.https://doi.org/10.1038/s41419-025-07961-x
spellingShingle Xuanbao Yao
Kehua Zhang
Tao Na
Yuchun Wang
Yuhan Guo
Jiajie Xi
Xiang Li
Shufang Meng
Miao Xu
Human iPSC-derived spinal neural progenitors enhance sensorimotor recovery in spinal cord-injured NOD-SCID mice via differentiation and microenvironment regulation
Cell Death and Disease
title Human iPSC-derived spinal neural progenitors enhance sensorimotor recovery in spinal cord-injured NOD-SCID mice via differentiation and microenvironment regulation
title_full Human iPSC-derived spinal neural progenitors enhance sensorimotor recovery in spinal cord-injured NOD-SCID mice via differentiation and microenvironment regulation
title_fullStr Human iPSC-derived spinal neural progenitors enhance sensorimotor recovery in spinal cord-injured NOD-SCID mice via differentiation and microenvironment regulation
title_full_unstemmed Human iPSC-derived spinal neural progenitors enhance sensorimotor recovery in spinal cord-injured NOD-SCID mice via differentiation and microenvironment regulation
title_short Human iPSC-derived spinal neural progenitors enhance sensorimotor recovery in spinal cord-injured NOD-SCID mice via differentiation and microenvironment regulation
title_sort human ipsc derived spinal neural progenitors enhance sensorimotor recovery in spinal cord injured nod scid mice via differentiation and microenvironment regulation
url https://doi.org/10.1038/s41419-025-07961-x
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