Expression and activation of peroxisome proliferator-activated receptors in growth plate chondrocytes

Peroxisome proliferator-activated receptor γ (PPAR-γ) is a nuclear hormone receptor that is involved in a wide range of cellular processes. Although it is known that PPAR-γ plays an important role in cell cycle control, inflammation, apoptotic cell death, and other cellular processes, the role of PP...

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Bibliographic Details
Published in:Journal of orthopaedic research 2005-09, Vol.23 (5), p.1139-1145
Main Authors: Shao, Yvonne Y., Wang, Lai, Hicks, David G., Tarr, Shannon, Ballock, R. Tracy
Format: Article
Language:English
Subjects:
Animals
bcl-2-Associated X Protein
Caspases - metabolism
Cell Differentiation - drug effects
Chondrocyte
Chondrocytes - chemistry
Chondrocytes - cytology
DNA Fragmentation
Growth plate
Growth Plate - cytology
Immunohistochemistry
Peroxisome proliferator activated receptors
PPAR
PPAR gamma - analysis
PPAR gamma - physiology
Proto-Oncogene Proteins c-bcl-2 - analysis
Rats
Rats, Sprague-Dawley
Thyroid hormone
Triiodothyronine - pharmacology
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Summary:Peroxisome proliferator-activated receptor γ (PPAR-γ) is a nuclear hormone receptor that is involved in a wide range of cellular processes. Although it is known that PPAR-γ plays an important role in cell cycle control, inflammation, apoptotic cell death, and other cellular processes, the role of PPAR-γ in the normal and pathological function of growth plate chondrocytes has not been investigated. The purpose of this study was to determine if PPARs are expressed in growth plate chondrocytes and to describe the biological effect of PPAR activation in these cells. The results demonstrate the presence of three PPAR isoforms (α, δ, and γ) in growth plate cartilage. Activation of PPAR-γ by ciglitazone in growth plate chondrocytes inhibits T 3 induced terminal differentiation and promotes apoptosis through increased levels of caspase 3/7 activity and decreased expression of the anti-apoptotic protein Bcl-2.
ISSN:0736-0266
1554-527X
DOI:10.1016/j.orthres.2005.02.011