ArticleJournal of cellular physiology2008
Hypoxic induction of UCP3 in the growth plate: UCP3 suppresses chondrocyte autophagy.
Article in Journal of cellular physiology, 2008. 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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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.
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.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Hypoxia-Inducible Factor 1 and Mitochondria: An Intimate Connection.Biomolecules · 2022Review
- HIF-1α in Osteoarthritis: From Pathogenesis to Therapeutic Implications.Frontiers in pharmacology · 2022Review
- The role of HIF proteins in maintaining the metabolic health of the intervertebral disc.Nature reviews. Rheumatology · 2021Review
- The Emerging Role of Glucose Metabolism in Cartilage Development.Current osteoporosis reports · 2019Review
- Ionizing radiation, ion transports, and radioresistance of cancer cells.Frontiers in physiology · 2013Article
- Article
- Numerical modeling of oxygen distributions in cortical and cancellous bone: oxygen availability governs osteonal and trabecular dimensions.American journal of physiology. Cell physiology · 2010Article
- Regulation of autophagy in human and murine cartilage: hypoxia-inducible factor 2 suppresses chondrocyte autophagy.Arthritis and rheumatism · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The overall goal of the investigation was to examine the role of uncoupling proteins (UCPs) in regulating late stage events in the chondrocyte maturation pathway. We showed for the first time that epiphyseal chondrocytes expressed UCP3. In hypoxia, UCP3 mediated regulation of the mitochondrial transmembrane potential (DeltaPsi(m)) was dependent on HIF-1alpha. We also showed for the first time that UCP3 regulated the induction of autophagy. Thus, suppression of UCP3 enhanced the expression of the autophagic phenotype, even in serum-replete media. Predictably, the mature autophagic chondrocytes were susceptible to an apoptogen challenge. Susceptibility was probably associated with a lowered expression of the anti-apoptotic proteins Bcl2 and BCL(xL) and a raised baseline expression of cytochrome c in the cytosol. These changes would serve to promote sensitivity to apoptogens. We conclude that in concert with HIF-1alpha, UCP3 regulates the activity of the mitochondrion by modulating the transmembrane potential. In addition, it inhibits induction of the autophagic response. When this occurs, it suppresses sensitivity to agents that promote chondrocyte deletion from the growth plate.
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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.