ArticleEuropean journal of histochemistry : EJH2014
Investigating conversion of endplate chondrocytes induced by intermittent cyclic mechanical unconfined compression in three-dimensional cultures.
Article in European journal of histochemistry : EJH, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Targeting skeletal interoception: a novel mechanistic insight into intervertebral disc degeneration and pain management.Journal of orthopaedic surgery and research · 2025Review
- Review
- Intermittent cyclic mechanical compression promotes endplate chondrocytes degeneration by disturbing Nrf2/PINK1 signaling pathway-dependent mitophagy.Human cell · 2023Article
- Lectin-like, oxidized low-density lipoprotein receptor-1-deficient mice show resistance to age-related knee osteoarthritis.European journal of histochemistry : EJH · 2017Article
- Is there still room for novelty, in histochemical papers?European journal of histochemistry : EJH · 2016Review
- The Role of ANK in Calcium Pyrophosphate Deposition Disease.Current rheumatology reports · 2016Review
- Histochemistry in biology and medicine: a message from the citing journals.European journal of histochemistry : EJH · 2015Review
- Impact of Histochemistry on biomedical research: looking through the articles published in a long-established histochemical journal.European journal of histochemistry : EJH · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mechanical stimulation is known to regulate the calcification of endplate chondrocytes. The ANK protein has a strong influence on anti-calcification by transports intracellular inorganic pyrophosphate (PPi) to the extracellular. It is known that TGF-β1 is able to induced Ank gene expression and protect chondrocyte calcification. Intermittent cyclic mechanical tension (ICMT) could induce calcification of endplate chondrocytes by decrease the expression of Ank gene. In this study, we investigated the relation of intermittent cyclic mechanical unconfined compression (ICMC) and Ank gene expression. We found that ICMC decreased the Ank gene expression in the endplate chondrocytes, and there was an decreased in the TGF-β1 expression after ICMC stimulation. The Ank gene expression significantly increased when treated by transforming growth factor alpha 1 (TGF-β1) in a dose-dependent manner and decreased when treated by SB431542 (ALK inhibitor) in a dose-dependent manner. Our results implicate that ICMC-induced downregulation of Ank gene expression may be regulated by TGF-β1 in endplate chondrocytes.
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Registered trials
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.