The single-cell transcription reveals the aberrant differentiation trajectory of chondrocytes in the intervertebral disc for congenital scoliosis
Cartilage endplate (CEP) in the intervertebral disc (IVD) contributes to vertebral level asymmetrically in congenital scoliosis (CS). However, the cellular compositions of CEP and the subsequent alteration of cellular environment in its neighboring annulus fibrosus and nucleus pulposus remain unknow...
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Published in | iScience Vol. 28; no. 6; p. 112608 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
20.06.2025
Elsevier |
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Online Access | Get full text |
ISSN | 2589-0042 2589-0042 |
DOI | 10.1016/j.isci.2025.112608 |
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Abstract | Cartilage endplate (CEP) in the intervertebral disc (IVD) contributes to vertebral level asymmetrically in congenital scoliosis (CS). However, the cellular compositions of CEP and the subsequent alteration of cellular environment in its neighboring annulus fibrosus and nucleus pulposus remain unknown during the progressive scoliosis. Herein, this study resolved the single-cell landscape of IVD in CS. Chondrocytes in CS demonstrated a different trajectory and were enriched in the cytoskeleton dependent cytokinesis pathways. H19, ECRG4, CCN1, and CCN2 were the specific markers for CS, and DBP may be the critical transcription factor (TF) for CS. Notochord and pericyte were the dominative cell types in the cell-cell communications, among which NCAM and SEMA5 signaling were the unique pathways for CS. Collectively, the aberrant differentiation trajectory of chondrocytes may explain the vertebral dysplasia in CS, and these critical gene markers, TFs, and pathways identified in this study may provide potential therapeutic targets for CS.
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•Chondrocytes in CS demonstrated a different differentiation trajectory•H19, ECRG4, CCN1, and CCN2 were the specific markers for CS•DBP may be the critical transcription factor for CS•Intercellular crosstalk identified the key roles of notochord and pericyte in CS
Pathophysiology; Transcriptomics |
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AbstractList | Cartilage endplate (CEP) in the intervertebral disc (IVD) contributes to vertebral level asymmetrically in congenital scoliosis (CS). However, the cellular compositions of CEP and the subsequent alteration of cellular environment in its neighboring annulus fibrosus and nucleus pulposus remain unknown during the progressive scoliosis. Herein, this study resolved the single-cell landscape of IVD in CS. Chondrocytes in CS demonstrated a different trajectory and were enriched in the cytoskeleton dependent cytokinesis pathways. H19, ECRG4, CCN1, and CCN2 were the specific markers for CS, and DBP may be the critical transcription factor (TF) for CS. Notochord and pericyte were the dominative cell types in the cell-cell communications, among which NCAM and SEMA5 signaling were the unique pathways for CS. Collectively, the aberrant differentiation trajectory of chondrocytes may explain the vertebral dysplasia in CS, and these critical gene markers, TFs, and pathways identified in this study may provide potential therapeutic targets for CS.
[Display omitted]
•Chondrocytes in CS demonstrated a different differentiation trajectory•H19, ECRG4, CCN1, and CCN2 were the specific markers for CS•DBP may be the critical transcription factor for CS•Intercellular crosstalk identified the key roles of notochord and pericyte in CS
Pathophysiology; Transcriptomics Cartilage endplate (CEP) in the intervertebral disc (IVD) contributes to vertebral level asymmetrically in congenital scoliosis (CS). However, the cellular compositions of CEP and the subsequent alteration of cellular environment in its neighboring annulus fibrosus and nucleus pulposus remain unknown during the progressive scoliosis. Herein, this study resolved the single-cell landscape of IVD in CS. Chondrocytes in CS demonstrated a different trajectory and were enriched in the cytoskeleton dependent cytokinesis pathways. H19, ECRG4, CCN1, and CCN2 were the specific markers for CS, and DBP may be the critical transcription factor (TF) for CS. Notochord and pericyte were the dominative cell types in the cell-cell communications, among which NCAM and SEMA5 signaling were the unique pathways for CS. Collectively, the aberrant differentiation trajectory of chondrocytes may explain the vertebral dysplasia in CS, and these critical gene markers, TFs, and pathways identified in this study may provide potential therapeutic targets for CS.Cartilage endplate (CEP) in the intervertebral disc (IVD) contributes to vertebral level asymmetrically in congenital scoliosis (CS). However, the cellular compositions of CEP and the subsequent alteration of cellular environment in its neighboring annulus fibrosus and nucleus pulposus remain unknown during the progressive scoliosis. Herein, this study resolved the single-cell landscape of IVD in CS. Chondrocytes in CS demonstrated a different trajectory and were enriched in the cytoskeleton dependent cytokinesis pathways. H19, ECRG4, CCN1, and CCN2 were the specific markers for CS, and DBP may be the critical transcription factor (TF) for CS. Notochord and pericyte were the dominative cell types in the cell-cell communications, among which NCAM and SEMA5 signaling were the unique pathways for CS. Collectively, the aberrant differentiation trajectory of chondrocytes may explain the vertebral dysplasia in CS, and these critical gene markers, TFs, and pathways identified in this study may provide potential therapeutic targets for CS. Cartilage endplate (CEP) in the intervertebral disc (IVD) contributes to vertebral level asymmetrically in congenital scoliosis (CS). However, the cellular compositions of CEP and the subsequent alteration of cellular environment in its neighboring annulus fibrosus and nucleus pulposus remain unknown during the progressive scoliosis. Herein, this study resolved the single-cell landscape of IVD in CS. Chondrocytes in CS demonstrated a different trajectory and were enriched in the cytoskeleton dependent cytokinesis pathways. H19, ECRG4, CCN1, and CCN2 were the specific markers for CS, and DBP may be the critical transcription factor (TF) for CS. Notochord and pericyte were the dominative cell types in the cell-cell communications, among which NCAM and SEMA5 signaling were the unique pathways for CS. Collectively, the aberrant differentiation trajectory of chondrocytes may explain the vertebral dysplasia in CS, and these critical gene markers, TFs, and pathways identified in this study may provide potential therapeutic targets for CS. Cartilage endplate (CEP) in the intervertebral disc (IVD) contributes to vertebral level asymmetrically in congenital scoliosis (CS). However, the cellular compositions of CEP and the subsequent alteration of cellular environment in its neighboring annulus fibrosus and nucleus pulposus remain unknown during the progressive scoliosis. Herein, this study resolved the single-cell landscape of IVD in CS. Chondrocytes in CS demonstrated a different trajectory and were enriched in the cytoskeleton dependent cytokinesis pathways. H19, ECRG4, CCN1, and CCN2 were the specific markers for CS, and DBP may be the critical transcription factor (TF) for CS. Notochord and pericyte were the dominative cell types in the cell-cell communications, among which NCAM and SEMA5 signaling were the unique pathways for CS. Collectively, the aberrant differentiation trajectory of chondrocytes may explain the vertebral dysplasia in CS, and these critical gene markers, TFs, and pathways identified in this study may provide potential therapeutic targets for CS. • Chondrocytes in CS demonstrated a different differentiation trajectory • H19, ECRG4, CCN1, and CCN2 were the specific markers for CS • DBP may be the critical transcription factor for CS • Intercellular crosstalk identified the key roles of notochord and pericyte in CS Pathophysiology; Transcriptomics |
ArticleNumber | 112608 |
Author | Li, Lin Fu, Dong Li, Haodong Wang, Junfeng Zheng, Yiming Qian, Chuang Qian, Maoxiang Wang, Dahui |
Author_xml | – sequence: 1 givenname: Junfeng surname: Wang fullname: Wang, Junfeng organization: Department of Orthopedics, Children’s Hospital of Fudan University, Shanghai 201102, P.R. China – sequence: 2 givenname: Haodong surname: Li fullname: Li, Haodong organization: Department of Orthopedics, Children’s Hospital of Fudan University, Shanghai 201102, P.R. China – sequence: 3 givenname: Dong surname: Fu fullname: Fu, Dong organization: Department of Orthopedics, Children’s Hospital of Fudan University, Shanghai 201102, P.R. China – sequence: 4 givenname: Yiming surname: Zheng fullname: Zheng, Yiming organization: Department of Orthopedics, Children’s Hospital of Fudan University, Shanghai 201102, P.R. China – sequence: 5 givenname: Chuang surname: Qian fullname: Qian, Chuang organization: Department of Orthopedics, Children’s Hospital of Fudan University, Shanghai 201102, P.R. China – sequence: 6 givenname: Lin surname: Li fullname: Li, Lin organization: Department of Hematology and Oncology, Children’s Hospital of Fudan University, and Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, P.R. China – sequence: 7 givenname: Maoxiang surname: Qian fullname: Qian, Maoxiang email: mxqian@fudan.edu.cn organization: Department of Hematology and Oncology, Children’s Hospital of Fudan University, and Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, P.R. China – sequence: 8 givenname: Dahui orcidid: 0000-0002-3101-702X surname: Wang fullname: Wang, Dahui email: wangdahui@fudan.edu.cn organization: Department of Orthopedics, Children’s Hospital of Fudan University, Shanghai 201102, P.R. China |
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Title | The single-cell transcription reveals the aberrant differentiation trajectory of chondrocytes in the intervertebral disc for congenital scoliosis |
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