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PPARγ and novel nuclear factors in the interplay between adipose tissue and the cardiovascular system: view from the chair

International Journal of Obesity volume 29, pages S24–S25 (2005)Cite this article

At four years after the Symposium on the ‘Recent advances in adipose tissue biology’, also organized in Quebec City by the DB Brown Research Chair on Obesity, we are now confronted with the fact that far more complex roles can be assigned to adipose tissue proteins. An impressive panel of speakers have highlighted the importance of nuclear proteins beyond their established respective function.

Dr Ron Law started the afternoon session on peroxisome proliferator-activated receptors (PPARs) and their novel targets in the vessel wall. Previous work from many groups have already established an important role of PPARγ in vessel wall macrophages through its implication in the transcription of genes involved in cholesterol homeostasis, macrophage differentiation, and inflammation.1 Law provided new data showing that PPARγ expressed in vascular smooth muscle cells (VSMC) is upregulated upon wall mechanical damage. His findings suggested that both PPARγ ligands and PPARγ overexpression inhibit the formation of the neointima by suppressing VSMC proliferation during the G1 to S phase transition. This suppression was due in part to the hypophosphorylation of Rb, a PPARγ corepressor that also inhibits the adipogenic action of the nuclear receptor (which was discussed earlier in the day by Lluis Fajas). PPARγ ligands also stimulate VSMC apoptosis through the induction of GADD45, a second nuclear receptor involved in cell survival. Law argued that his findings are consistent with the impact of PPARγ ligands such as troglitazone or rosiglitazone on neointimal tissue formation after coronary stent implantation in diabetic patients with macrovascular disease, although the effect of PPARγ ligands on VSMC cells per se has not been determined in the clinic. His data added new concepts to the controversial effects of PPARγ on angiogenesis, in which VSMC proliferation probably plays an active contribution. The use of PPARγ knockin, knockout, and transgenic mice could shed more light on this process.

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  1. Laval Hospital Research Center, Faculty of Pharmacy, Université Laval, Quebec, QC, Canada

    F Picard & Y Deshaies

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  1. F Picard
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Correspondence to F Picard.

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Picard, F., Deshaies, Y. PPARγ and novel nuclear factors in the interplay between adipose tissue and the cardiovascular system: view from the chair. Int J Obes 29 (Suppl 1), S24–S25 (2005). https://doi.org/10.1038/sj.ijo.0802909

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