Evidence map›Paper›PMID 28983104›Full record

ArticleScientific reports2017

SHP2 Regulates the Osteogenic Fate of Growth Plate Hypertrophic Chondrocytes.

Lijun Wang, Jiahui Huang, Douglas C Moore, Chunlin Zuo, Qian Wu, Liqin Xie, Klaus von der Mark, Xin Yuan, Di Chen, Matthew L Warman and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.1field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. SHP2 ablation mitigates osteoarthritic cartilage degeneration by promoting chondrocyte anabolism through SOX9.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. From Stem to Sternum: The Role of Shp2 in the Skeleton.Calcified tissue international · 2023
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. A comprehensive review of SHP2 and its role in cancer.Cellular oncology (Dordrecht, Netherlands) · 2022
    Review
  16. Review
  17. Article
  18. Article
  19. Enchondromatosis and Growth Plate Development.Current osteoporosis reports · 2021
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 8 institutions in 3 countries.

Lijun WangDepartment of Orthopaedic Surgery, Brown University Alpert Medical School, Providence, RI, 02903, USA.
Jiahui HuangDepartment of Orthopaedic Surgery, Brown University Alpert Medical School, Providence, RI, 02903, USA.
Douglas C MooreDepartment of Orthopaedic Surgery, Brown University Alpert Medical School, Providence, RI, 02903, USA.
Chunlin ZuoDepartment of Orthopaedic Surgery, Brown University Alpert Medical School, Providence, RI, 02903, USA.
Qian WuDepartment of Pathology and Laboratory Medicine, University of Connecticut Health Center, Farmington, CT, 06030, USA.
Liqin XieRegeneron Pharmaceuticals, Tarrytown, NY, 10591, USA.
Klaus von der MarkDepartment of Experimental Medicine, University of Erlangen-Nürnberg, Gluckstrasse 6, 91054, Erlangen, Germany.
Xin YuanDepartment of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, 02115, USA.
Di ChenDepartment of Biochemistry, Rush University, 600 S. Paulina St., Chicago, IL, 60612, USA.
Matthew L WarmanOrthopaedic Research Laboratories and Howard Hughes Medical Institute, Boston Children's Hospital and Harvard Medical School, Boston, MA, 02115, USA.ORCID 0000-0003-2020-3449
Michael G EhrlichDepartment of Orthopaedic Surgery, Brown University Alpert Medical School, Providence, RI, 02903, USA.
Wentian YangDepartment of Orthopaedic Surgery, Brown University Alpert Medical School, Providence, RI, 02903, USA. wyang@lifespan.org.
Brown University · USAnhui Medical University · CNBeth Israel Deaconess Medical Center · USBoston Children's Hospital · USFriedrich-Alexander-Universität Erlangen-Nürnberg · DERegeneron (United States) · USRush University · USUConn Health · US

Funding

COBRE for Skeletal Health and RepairP20GM104937 · NIGMS · RHODE ISLAND HOSPITAL · PI CHEN, QIAN · 2012 to 2016
$10.8M
Pilot Projects ProgramP30GM122732 · NIGMS · RHODE ISLAND HOSPITAL · PI CHEN, QIAN · 2017 to 2021
$6.6M
Stem Cell Biology: New Directions in Clinical and Basic ResearchP20GM103468 · NIGMS · RHODE ISLAND HOSPITAL · PI QUESENBERRY, PETER J. · 2012 to 2013
$4.5M
Role of PTPN11 in Cartilage Stem Cells and TumorigenesisR01AR066746 · NIAMS · RHODE ISLAND HOSPITAL · PI YANG, WENTIAN · 2015 to 2019
$1.8M
Shp2 in Osteoclastogenesis and Bone RemodelingR21AR057156 · NIAMS · RHODE ISLAND HOSPITAL · PI YANG, WENTIAN · 2009 to 2010
$378k
NIAMS NIH HHS R01 AR066746NIAMS NIH HHS R21 AR057156NIGMS NIH HHS P20 GM103468NIGMS NIH HHS P20 GM104937NIGMS NIH HHS P30 GM122732
6 · The paper itself

Abstract

Transdifferentiation of hypertrophic chondrocytes into bone-forming osteoblasts has been reported, yet the underlying molecular mechanism remains incompletely understood. SHP2 is an ubiquitously expressed cytoplasmic protein tyrosine phosphatase. SHP2 loss-of-function mutations in chondroid cells are linked to metachondromatosis in humans and mice, suggesting a crucial role for SHP2 in the skeleton. However, the specific role of SHP2 in skeletal cells has not been elucidated. To approach this question, we ablated SHP2 in collagen 2α1(Col2α1)-Cre- and collagen 10α1(Col10α1)-Cre-expressing cells, predominantly proliferating and hypertrophic chondrocytes, using "Cre-loxP"-mediated gene excision. Mice lacking SHP2 in Col2α1-Cre-expressing cells die at mid-gestation. Postnatal SHP2 ablation in the same cell population caused dwarfism, chondrodysplasia and exostoses. In contrast, mice in which SHP2 was ablated in the Col10α1-Cre-expressing cells appeared normal but were osteopenic. Further mechanistic studies revealed that SHP2 exerted its influence partly by regulating the abundance of SOX9 in chondrocytes. Elevated and sustained SOX9 in SHP2-deficient hypertrophic chondrocytes impaired their differentiation to osteoblasts and impaired endochondral ossification. Our study uncovered an important role of SHP2 in bone development and cartilage homeostasis by influencing the osteogenic differentiation of hypertrophic chondrocytes and provided insight into the pathogenesis and potential treatment of skeletal diseases, such as osteopenia and osteoporosis.

Indexed as

AnimalsBone DevelopmentBone NeoplasmsCartilageCell DifferentiationCell ProliferationCell TransdifferentiationChondrocytesChondrogenesisChondromatosisExostoses, Multiple HereditaryGrowth PlateHumansHypertrophyMiceOsteoblastsProtein Tyrosine Phosphatase, Non-Receptor Type 11SOX9 protein, humanSOX9 Transcription Factor

Identifiers

PMID28983104
PMCPMC5629218
OpenAlexW2758808877

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.