Single cell analysis of Idh mutant growth plates identifies cell populations responsible for longitudinal bone growth and enchondroma formation.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
31 Oct 2024
Historique:
received: 20 05 2024
accepted: 15 10 2024
medline: 1 11 2024
pubmed: 1 11 2024
entrez: 1 11 2024
Statut: epublish

Résumé

Enchondromas are a common tumor in bone that can occur as multiple lesions in enchondromatosis, which is associated with deformity of the affected bone. These lesions harbor somatic mutations in IDH and driving expression of a mutant Idh1 in Col2 expressing cells in mice causes an enchondromatosis phenotype. Here we compared growth plates from E18.5 mice expressing a mutant Idh1 with control littermates using single cell RNA sequencing. Data from Col2 expressing cells were analysed using UMAP and RNA pseudo-time analyses. A unique cluster of cells was identified in the mutant growth plates that expressed genes known to be upregulated in enchondromas. There was also a cluster of cells that was underrepresented in the mutant growth plates that expressed genes known to be important in longitudinal bone growth. Immunofluorescence showed that the genes from the unique cluster identified in the mutant growth plates were expressed in multiple growth plate anatomic zones, and pseudo-time analysis also suggested these cells could arise from multiple growth plate chondrocyte subpopulations. This data supports the notion that a subpopulation of chondrocytes become enchondromas at the expense of contributing to longitudinal growth.

Identifiants

pubmed: 39482341
doi: 10.1038/s41598-024-76539-y
pii: 10.1038/s41598-024-76539-y
doi:

Substances chimiques

Isocitrate Dehydrogenase EC 1.1.1.41
Collagen Type II 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

26208

Subventions

Organisme : NIH HHS
ID : R01 AR066765
Pays : United States
Organisme : NIH HHS
ID : R01 AR066765
Pays : United States

Informations de copyright

© 2024. The Author(s).

Références

Hong, E. D. et al. Prevalence of shoulder enchondromas on routine MR imaging. Clin. Imaging. 35 (5), 378–384 (2011).
pubmed: 21872128 doi: 10.1016/j.clinimag.2010.10.012
Walden, M. J., Murphey, M. D. & Vidal, J. A. Incidental enchondromas of the knee. AJR Am. J. Roentgenol. 190 (6), 1611–1615 (2008).
pubmed: 18492914 doi: 10.2214/AJR.07.2796
Amary, M. F. et al. IDH1 and IDH2 mutations are frequent events in central chondrosarcoma and central and periosteal chondromas but not in other mesenchymal tumours. J. Pathol. 224 (3), 334–343 (2011).
pubmed: 21598255 doi: 10.1002/path.2913
Pansuriya, T. C. et al. Somatic mosaic IDH1 and IDH2 mutations are associated with enchondroma and spindle cell hemangioma in Ollier disease and Maffucci syndrome. Nat. Genet. 43 (12), 1256–1261 (2011).
pubmed: 22057234 pmcid: 3427908 doi: 10.1038/ng.1004
Hirata, M. et al. Mutant IDH is sufficient to initiate enchondromatosis in mice. Proc. Natl. Acad. Sci. U S A. 112 (9), 2829–2834 (2015).
pubmed: 25730874 pmcid: 4352794 doi: 10.1073/pnas.1424400112
Dang, L. et al. Cancer-associated IDH1 mutations produce 2-hydroxyglutarate. Nature. 465 (7300), 966 (2010).
pubmed: 20559394 pmcid: 3766976 doi: 10.1038/nature09132
Marcucci, G. et al. IDH1 and IDH2 gene mutations identify novel molecular subsets within de novo cytogenetically normal acute myeloid leukemia: a Cancer and Leukemia Group B study. J. Clin. Oncol. 28 (14), 2348–2355 (2010).
pubmed: 20368543 pmcid: 2881719 doi: 10.1200/JCO.2009.27.3730
Yan, H. et al. IDH1 and IDH2 mutations in gliomas. N Engl. J. Med. 360 (8), 765–773 (2009).
pubmed: 19228619 pmcid: 2820383 doi: 10.1056/NEJMoa0808710
Zhao, S. et al. Glioma-derived mutations in IDH1 dominantly inhibit IDH1 catalytic activity and induce HIF-1alpha. Science. 324 (5924), 261–265 (2009).
pubmed: 19359588 pmcid: 3251015 doi: 10.1126/science.1170944
Figueroa, M. E. et al. Leukemic IDH1 and IDH2 mutations result in a hypermethylation phenotype, disrupt TET2 function, and impair hematopoietic differentiation. Cancer Cell 18 (6), 553–567 (2010).
pubmed: 21130701 pmcid: 4105845 doi: 10.1016/j.ccr.2010.11.015
Turcan, S. et al. IDH1 mutation is sufficient to establish the glioma hypermethylator phenotype. Nature. 483 (7390), 479–483 (2012).
pubmed: 22343889 pmcid: 3351699 doi: 10.1038/nature10866
Xu, W. et al. Oncometabolite 2-hydroxyglutarate is a competitive inhibitor of alpha-ketoglutarate-dependent dioxygenases. Cancer Cell 19 (1), 17–30 (2011).
pubmed: 21251613 pmcid: 3229304 doi: 10.1016/j.ccr.2010.12.014
Lu, C. et al. Induction of sarcomas by mutant IDH2. Genes Dev. 27 (18), 1986–1998 (2013).
pubmed: 24065766 pmcid: 3792475 doi: 10.1101/gad.226753.113
Zhang, H. et al. Intracellular cholesterol biosynthesis in enchondroma and chondrosarcoma. JCI Insight, 5  (11). (2019).
Zhang, H. et al. Distinct roles of glutamine metabolism in Benign and malignant cartilage tumors with IDH mutations. J. Bone Min. Res. 37 (5), 983–996 (2022).
doi: 10.1002/jbmr.4532
DiFrisco, J., Love, A. C. & Wagner, G. P. Character identity mechanisms: a conceptual model for comparative-mechanistic biology. Biol. Philos. 35 (4), 44 (2020).
doi: 10.1007/s10539-020-09762-2
Kobayashi, T. et al. Indian hedgehog stimulates periarticular chondrocyte differentiation to regulate growth plate length independently of PTHrP. J. Clin. Invest. 115 (7), 1734–1742 (2005).
pubmed: 15951842 pmcid: 1143590 doi: 10.1172/JCI24397
Lefebvre, V. & Smits, P. Transcriptional control of chondrocyte fate and differentiation. Birth Defects Res. C Embryo Today. 75 (3), 200–212 (2005).
pubmed: 16187326 doi: 10.1002/bdrc.20048
Tagariello, A. et al. Ucma—a novel secreted factor represents a highly specific marker for distal chondrocytes. Matrix Biol. 27 (1), 3–11 (2008).
pubmed: 17707622 doi: 10.1016/j.matbio.2007.07.004
Eitzinger, N. et al. Ucma is not necessary for normal development of the mouse skeleton. Bone. 50 (3), 670–680 (2012).
pubmed: 22155508 doi: 10.1016/j.bone.2011.11.017
Kato, K. et al. SOXC transcription factors induce cartilage growth plate formation in mouse embryos by promoting noncanonical WNT signaling. J. Bone Min. Res. 30 (9), 1560–1571 (2015).
doi: 10.1002/jbmr.2504
Surmann-Schmitt, C. et al. Wif-1 is expressed at cartilage-mesenchyme interfaces and impedes Wnt3a-mediated inhibition of chondrogenesis. J. Cell. Sci. 122 (Pt 20), 3627–3637 (2009).
pubmed: 19755491 doi: 10.1242/jcs.048926
Li, J. et al. Systematic reconstruction of molecular cascades regulating GP development using single-cell RNA-Seq. Cell Rep. 15 (7), 1467–1480 (2016).
pubmed: 27160914 doi: 10.1016/j.celrep.2016.04.043
Zhang, C. H. et al. Creb5 establishes the competence for Prg4 expression in articular cartilage. Commun. Biol. 4 (1), 332 (2021).
pubmed: 33712729 pmcid: 7955038 doi: 10.1038/s42003-021-01857-0
Ng, J. Q. et al. Loss of Grem1-lineage chondrogenic progenitor cells causes osteoarthritis. Nat. Commun. 14 (1), 6909 (2023).
pubmed: 37907525 pmcid: 10618187 doi: 10.1038/s41467-023-42199-1
Liddiard, K. et al. DNA ligase 1 is an essential mediator of sister chromatid telomere fusions in G2 cell cycle phase. Nucleic Acids Res. 47 (5), 2402–2424 (2019).
pubmed: 30590694 doi: 10.1093/nar/gky1279
Koltes, J. E. et al. Transcriptional profiling of PRKG2-null growth plate identifies putative down-stream targets of PRKG2. BMC Res. Notes. 8, 177 (2015).
pubmed: 25924610 pmcid: 4419418 doi: 10.1186/s13104-015-1136-6
Akiyama, H. et al. Indian hedgehog in the late-phase differentiation in mouse chondrogenic EC cells, ATDC5: upregulation of type X collagen and osteoprotegerin ligand mRNAs. Biochem. Biophys. Res. Commun. 257 (3), 814–820 (1999).
pubmed: 10208865 doi: 10.1006/bbrc.1999.0494
Zheng, Q. et al. Type X collagen gene regulation by Runx2 contributes directly to its hypertrophic chondrocyte-specific expression in vivo. J. Cell. Biol. 162 (5), 833–842 (2003).
pubmed: 12952936 pmcid: 2172833 doi: 10.1083/jcb.200211089
Nakashima, K. et al. The novel zinc finger-containing transcription factor osterix is required for osteoblast differentiation and bone formation. Cell 108 (1), 17–29 (2002).
pubmed: 11792318 doi: 10.1016/S0092-8674(01)00622-5
Qin, X. et al. Runx2 is essential for the transdifferentiation of chondrocytes into osteoblasts. PLoS Genet. 16 (11), e1009169 (2020).
pubmed: 33253203 pmcid: 7728394 doi: 10.1371/journal.pgen.1009169
See, P. et al. A single-cell sequencing guide for immunologists. Front. Immunol. 9, 2425 (2018).
pubmed: 30405621 pmcid: 6205970 doi: 10.3389/fimmu.2018.02425
Suzuki, N. et al. Teneurin-4, a transmembrane protein, is a novel regulator that suppresses chondrogenic differentiation. J. Orthop. Res. 32 (7), 915–922 (2014).
pubmed: 24648313 doi: 10.1002/jor.22616
Matsumoto, M. et al. Targeted deletion of the murine corneodesmosin gene delineates its essential role in skin and hair physiology. Proc. Natl. Acad. Sci. 105 (18), 6720–6724 (2008).
pubmed: 18436651 pmcid: 2373361 doi: 10.1073/pnas.0709345105
Witte, F. et al. Comprehensive expression analysis of all wnt genes and their major secreted antagonists during mouse limb development and cartilage differentiation. Gene Expr. Patterns 9 (4), 215–223 (2009).
pubmed: 19185060 doi: 10.1016/j.gep.2008.12.009
Jonca, N. et al. Corneodesmosomes and corneodesmosin: from the stratum corneum cohesion to the pathophysiology of genodermatoses. Eur. J. Dermatol. 21 (Suppl 2), 35–42 (2011).
pubmed: 21628128
Karna, E. et al. Proline-dependent regulation of collagen metabolism. Cell. Mol. Life Sci. 77 (10), 1911–1918 (2020).
pubmed: 31740988 doi: 10.1007/s00018-019-03363-3
Yao, B. et al. Investigating the molecular control of deer antler extract on articular cartilage. J. Orthop. Surg. Res. 16 (1), 8 (2021).
pubmed: 33407721 pmcid: 7788833 doi: 10.1186/s13018-020-02148-w
Li, Y., Yang, S. T. & Yang, S. Trp53 controls chondrogenesis and endochondral ossification by negative regulation of TAZ activity and stability via beta-TrCP-mediated ubiquitination. Cell. Death Discov. 8 (1), 317 (2022).
pubmed: 35831272 pmcid: 9279315 doi: 10.1038/s41420-022-01105-2
Surmann-Schmitt, C. et al. Ucma, a Novel secreted cartilage-specific protein with implications in osteogenesis*. J. Biol. Chem. 283 (11), 7082–7093 (2008).
pubmed: 18156182 doi: 10.1074/jbc.M702792200
Trainor, P. A. & Merrill, A. E. Ribosome biogenesis in skeletal development and the pathogenesisof skeletal disorders. Biochim. Biophys. Acta Mol. Basis Dis. 1842 (6), 769–778 (2014).
doi: 10.1016/j.bbadis.2013.11.010
Shi, Z. et al. Exploring the key genes and pathways in enchondromas using a gene expression microarray. Oncotarget. 8 (27), 43967–43977 (2017).
pubmed: 28410203 pmcid: 5546454 doi: 10.18632/oncotarget.16700
Al-Jazrawe, M. et al. CD142 identifies neoplastic desmoid tumor cells, uncovering interactions between neoplastic and stromal cells that drive proliferation. Cancer Res. Commun. 3 (4), 697–708 (2023).
pubmed: 37377751 pmcid: 10128091 doi: 10.1158/2767-9764.CRC-22-0403
Long, F. et al. Genetic manipulation of hedgehog signaling in the endochondral skeleton reveals a direct role in the regulation of chondrocyte proliferation. Development. 128 (24), 5099–5108 (2001).
pubmed: 11748145 doi: 10.1242/dev.128.24.5099
Villani, A. C. et al. Single-cell RNA-seq reveals new types of human blood dendritic cells, monocytes, and progenitors. Science. 356 (6335) (2017).
Macosko, E. Z. et al. Highly parallel genome-wide expression profiling of individual cells using nanoliter droplets. Cell 161 (5), 1202–1214 (2015).
pubmed: 26000488 doi: 10.1016/j.cell.2015.05.002
Finak, G. et al. MAST: a flexible statistical framework for assessing transcriptional changes and characterizing heterogeneity in single-cell RNA sequencing data. Genome Biol. 16, 278 (2015).
pubmed: 26653891 pmcid: 4676162 doi: 10.1186/s13059-015-0844-5
Cao, J. et al. The single-cell transcriptional landscape of mammalian organogenesis. Nature. 566 (7745), 496–502 (2019).
pubmed: 30787437 pmcid: 6434952 doi: 10.1038/s41586-019-0969-x
Dobin, A. et al. STAR: ultrafast universal RNA-seq aligner. Bioinformatics. 29 (1), 15–21 (2013).
pubmed: 23104886 doi: 10.1093/bioinformatics/bts635
Liao, Y., Smyth, G. K. & Shi, W. featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. Bioinformatics. 30 (7), 923–930 (2014).
pubmed: 24227677 doi: 10.1093/bioinformatics/btt656
Love, M. I., Huber, W. & Anders, S. Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2. Genome Biol. 15 (12), 550 (2014).
pubmed: 25516281 pmcid: 4302049 doi: 10.1186/s13059-014-0550-8
Yu, G. et al. clusterProfiler: an R package for comparing biological themes among gene clusters. Omics. 16 (5), 284–287 (2012).
pubmed: 22455463 pmcid: 3339379 doi: 10.1089/omi.2011.0118
Ramírez, F. et al. deepTools2: a next generation web server for deep-sequencing data analysis. Nucleic Acids Res. 44 (W1), W160–W165 (2016).
pubmed: 27079975 pmcid: 4987876 doi: 10.1093/nar/gkw257
Patro, R. et al. Salmon provides fast and bias-aware quantification of transcript expression. Nat. Methods. 14 (4), 417–419 (2017).
pubmed: 28263959 pmcid: 5600148 doi: 10.1038/nmeth.4197

Auteurs

Vijitha Puviindran (V)

Department of Orthopedic Surgery, Duke University School of Medicine, Durham, NC, USA.

Eijiro Shimada (E)

Department of Orthopedic Surgery, Duke University School of Medicine, Durham, NC, USA.

Zeyu Huang (Z)

Department of Orthopedic Surgery, Duke University School of Medicine, Durham, NC, USA.

Xinyi Ma (X)

Department of Orthopedic Surgery, Duke University School of Medicine, Durham, NC, USA.
Department of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, NC, USA.
Developmental and Stem Cell Biology Program, Duke University School of Medicine, Durham, NC, USA.

Ga I Ban (GI)

Department of Orthopedic Surgery, Duke University School of Medicine, Durham, NC, USA.

Yu Xiang (Y)

Department of Cell Biology, Duke University School of Medicine, Durham, NC, USA.
Regeneration Center, Duke University School of Medicine, Durham, NC, USA.

Hongyuan Zhang (H)

Department of Orthopedic Surgery, Duke University School of Medicine, Durham, NC, USA.
Department of Cell Biology, Duke University School of Medicine, Durham, NC, USA.

Jianhong Ou (J)

Regeneration Center, Duke University School of Medicine, Durham, NC, USA.

Xiaolin Wei (X)

Department of Cell Biology, Duke University School of Medicine, Durham, NC, USA.
Regeneration Center, Duke University School of Medicine, Durham, NC, USA.

Makoto Nakagawa (M)

Department of Orthopedic Surgery, Duke University School of Medicine, Durham, NC, USA.

John Martin (J)

Department of Orthopedic Surgery, Duke University School of Medicine, Durham, NC, USA.

Yarui Diao (Y)

Department of Orthopedic Surgery, Duke University School of Medicine, Durham, NC, USA.
Department of Cell Biology, Duke University School of Medicine, Durham, NC, USA.
Regeneration Center, Duke University School of Medicine, Durham, NC, USA.

Benjamin A Alman (BA)

Department of Orthopedic Surgery, Duke University School of Medicine, Durham, NC, USA. ben.alman@duke.edu.
Department of Cell Biology, Duke University School of Medicine, Durham, NC, USA. ben.alman@duke.edu.
Regeneration Center, Duke University School of Medicine, Durham, NC, USA. ben.alman@duke.edu.
Department of Pharmacology and Cancer Biology, Duke University School of Medicine, Durham, NC, USA. ben.alman@duke.edu.
Developmental and Stem Cell Biology Program, Duke University School of Medicine, Durham, NC, USA. ben.alman@duke.edu.

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