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Research Article | Open Access

Volume 2006 |Article ID 067297 | https://doi.org/10.1155/PPAR/2006/67297

Lai Wang, Yvonne Y. Shao, R. Tracy Ballock, "Peroxisome Proliferator-Activated Receptor-γ Promotes Adipogenic Changes in Growth Plate Chondrocytes In Vitro", PPAR Research, vol. 2006, Article ID 067297, 8 pages, 2006. https://doi.org/10.1155/PPAR/2006/67297

Peroxisome Proliferator-Activated Receptor-γ Promotes Adipogenic Changes in Growth Plate Chondrocytes In Vitro

Received09 Apr 2006
Revised08 Jul 2006
Accepted10 Jul 2006
Published13 Sep 2006


Chondrocytes and adipocytes are two differentiated cell types which are both derived from mesenchymal cells. The purpose of this study was to investigate whether peroxisome proliferator-activated receptor-γ (PPARγ), a transcription factor involved in lineage determination during adipogenesis, is able to induce adipogenic differentiation in growth plate chondrocytes. Isolated epiphyseal chondrocytes were infected with a PPARγ adenovirus or treated with the PPARγ agonist ciglitazone. Both of these treatments resulted in lipid droplet accumulation and expression of the adipogenic markers aP2, lipoprotein lipase, and adipsin in chondrocytes. Proteoglycan matrix synthesis was decreased in the PPARγ-infected cells, as was the expression of the chondrogenic genes Col2a1 and aggrecan. Growth plate cells transfected with a PPARγ expression plasmid under the control of the collagen α1(II) promoter also demonstrated a similar adipogenic changes. Terminal differentiation of growth plate chondrocytes induced by thyroid hormone was also inhibited by overexpression of PPARγ and ciglitazone treatment, with decreased expression of alkaline phosphatase and Runx2/Cbfa1 genes. These in vitro data suggest that PPARγ is able to promote adipogenic differentiation in growth plate chondrocytes, while negatively regulating chondrogenic differentiation and terminal differentiation.


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Copyright © 2006 Lai Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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