Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 216, Issue 2, Pages 419-425Publisher
WILEY
DOI: 10.1002/jcp.21408
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Funding
- NIDCR NIH HHS [R03 DE015694, R01 DE013319-01, R03 DE015694-01, R01 DE016383, DE 013319, R01 DE010875-06, DE 010875, R01 DE016383-01, DE 016383, R01 DE013319, DE 015694, R01 DE010875] Funding Source: Medline
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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 (Delta Psi(m)) was dependent on HIF-1 alpha. 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 BCLxL 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-1 alpha, 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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