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

• Published in: Journal of orthopaedic research Vol. 23; no. 5; pp. 1139 - 1145
• Main Authors: Shao, Yvonne Y., Wang, Lai, Hicks, David G., Tarr, Shannon, Ballock, R. Tracy
• Format: Journal Article
• Language: English
• Published: Hoboken Elsevier Ltd 01.09.2005; Wiley Subscription Services, Inc., A Wiley Company; Blackwell Publishing Ltd
• 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; Peroxisome proliferator activated receptors; Growth plate; Thyroid hormone; Chondrocyte; PPAR
• ISSN: 0736-0266; 1554-527X
• DOI: 10.1016/j.orthres.2005.02.011

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.