Evidence map›Paper›PMID 37100374›Full record

ArticleOsteoarthritis and cartilage2023

Yes-associated protein nuclear translocation promotes anabolic activity in human articular chondrocytes.

Y Cui, M Z Miao, M Wang, Q P Su, K Qiu, L Arbeeva, S Chubinskaya, B O Diekman, R F Loeser

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Osteoarthritis and cartilage, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Exercise-myokine relationships in osteoarthritis.Journal of translational medicine · 2026
    Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Osmolarity-Induced Altered Intracellular Molecular Crowding Drives Osteoarthritis Pathology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  13. 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

9 authors at 3 institutions in 3 countries.

Y CuiXiangya International Medical Center, Xiangya Hospital, Central South University, Changsha, Hunan Province, 410008, China; Thurston Arthritis Research Center, University of North Carolina School of Medicine, Chapel Hill, NC, 27599, USA. Electronic address: cuiyang@csu.edu.cn.
M Z MiaoThurston Arthritis Research Center, University of North Carolina School of Medicine, Chapel Hill, NC, 27599, USA; Division of Oral & Craniofacial Health Sciences, University of North Carolina Adams School of Dentistry, Chapel Hill, NC, 27599, USA. Electronic address: zhemiao@unc.edu.
M WangDivision of Pharmacoengineering and Molecular Pharmaceutics, University of North Carolina Eshelman School of Pharmacy, Chapel Hill, NC, 27599, USA. Electronic address: menglin@email.unc.edu.
Q P SuSchool of Biomedical Engineering, Faculty of Engineering and Information Technology, University of Technology Sydney, Sydney, NSW, 2007, Australia. Electronic address: qian.su@uts.edu.au.
K QiuDivision of Pharmacoengineering and Molecular Pharmaceutics, University of North Carolina Eshelman School of Pharmacy, Chapel Hill, NC, 27599, USA. Electronic address: kunyuqiu2017@outlook.com.
L ArbeevaThurston Arthritis Research Center, University of North Carolina School of Medicine, Chapel Hill, NC, 27599, USA. Electronic address: liubov_arbeeva@med.unc.edu.
S ChubinskayaDepartment of Pediatrics, Rush University Medical Center, Chicago, IL, 60612, USA. Electronic address: susanna_chubinskaya@rush.edu.
B O DiekmanThurston Arthritis Research Center, University of North Carolina School of Medicine, Chapel Hill, NC, 27599, USA; Joint Department of Biomedical Engineering, University of North Carolina at Chapel Hill and North Carolina State University, Raleigh, NC, 27599, USA. Electronic address: bdiekman@email.unc.edu.
R F LoeserThurston Arthritis Research Center, University of North Carolina School of Medicine, Chapel Hill, NC, 27599, USA. Electronic address: richard_loeser@med.unc.edu.
University of North Carolina at Chapel Hill · USRush University Medical Center · USUniversity of Technology Sydney · AU

Funding

Integrin Function in CartilageR37AR049003 · NIAMS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LOESER, RICHARD F · 2012 to 2021
$4.1M
Integrin Function in CartilageR01AR049003 · NIAMS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LOESER, RICHARD F · 2002 to 2011
$2.8M
NIAMS NIH HHS R01 AR049003NIAMS NIH HHS R37 AR049003
6 · The paper itself

Abstract

objectiveYes-associated protein (YAP) has been widely studied as a mechanotransducer in many cell types, but its function in cartilage is controversial. The aim of this study was to identify the effect of YAP phosphorylation and nuclear translocation on the chondrocyte response to stimuli relevant to osteoarthritis (OA).

designCultured normal human articular chondrocytes from 81 donors were treated with increased osmolarity media as an in vitro model of mechanical stimulation, fibronectin fragments (FN-f) or IL-1β as catabolic stimuli, and IGF-1 as an anabolic stimulus. YAP function was assessed with gene knockdown and inhibition by verteporfin. Nuclear translocation of YAP and its transcriptional co-activator TAZ and site-specific YAP phosphorylation were determined by immunoblotting. Immunohistochemistry and immunofluorescence to detect YAP were performed on normal and OA human cartilage with different degrees of damage.

resultsChondrocyte YAP/TAZ nuclear translocation increased under physiological osmolarity (400 mOsm) and IGF-1 stimulation, which was associated with YAP phosphorylation at Ser128. In contrast, catabolic stimulation decreased the levels of nuclear YAP/TAZ through YAP phosphorylation at Ser127. Following YAP inhibition, anabolic gene expression and transcriptional activity decreased. Additionally, YAP knockdown reduced proteoglycan staining and levels of type II collagen. Total YAP immunostaining was greater in OA cartilage, but YAP was sequestered in the cytosol in cartilage areas with more severe damage.

conclusionsYAP chondrocyte nuclear translocation is regulated by differential phosphorylation in response to anabolic and catabolic stimuli. Decreased nuclear YAP in OA chondrocytes may contribute to reduced anabolic activity and promotion of further cartilage loss.

Indexed as

Cartilage, ArticularOsteoarthritisYAP-Signaling ProteinsCell Cycle ProteinsCells, CulturedChondrocytesHumansInsulin-Like Growth Factor ITranscription FactorsCell Cycle ProteinsInsulin-Like Growth Factor ITranscription FactorsYAP-Signaling ProteinsYY1AP1 protein, humanChondrocytesDifferential phosphorylationMechanotransductionNuclear translocationYes-associated protein

Identifiers

PMID37100374
PMCPMC10524185
OpenAlexW4366824938

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

None linked

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.