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. 2006 Sep 20;2006:67297. doi: 10.1155/PPAR/2006/67297

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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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Inhibition of T3-induced hypertrophy and mineralization in the growth plate cells by PPARγ overexpression or ciglitazone treatment. (a) Growth plate cells were treated with T3 (100 ng/mL) in the presence or absence of ciglitazone (5 μM) for 10 days. Alkaline phosphatase (ALP) staining was used as a marker of terminal differentiation of growth plate chondrocytes. Positive stainings were colored in dark blue. Negative-stained background was colored in light green. (b) Quantitative PCR analysis of ALP and Runx2 genes 4 days after growth plate cells were infected with Ad-PPARγ or treated with ciglitazone. Ad-Gal-infected cells without T3 or ciglitazone treatment were used as controls. Gene expression levels were normalized with respect to endogenous 18S rRNA. * P < .05 versus the expression in the Ad-Gal-infected cells with T3-treatment.

Inhibition of T3-induced hypertrophy and mineralization in the growth plate cells by PPARγ overexpression or ciglitazone treatment. (a) Growth plate cells were treated with T3 (100 ng/mL) in the presence or absence of ciglitazone (5 μM) for 10 days. Alkaline phosphatase (ALP) staining was used as a marker of terminal differentiation of growth plate chondrocytes. Positive stainings were colored in dark blue. Negative-stained background was colored in light green. (b) Quantitative PCR analysis of ALP and Runx2 genes 4 days after growth plate cells were infected with Ad-PPARγ or treated with ciglitazone. Ad-Gal-infected cells without T3 or ciglitazone treatment were used as controls. Gene expression levels were normalized with respect to endogenous 18S rRNA. * P < .05 versus the expression in the Ad-Gal-infected cells with T3-treatment.