C/EBPα induces adipogenesis through PPARγ: a unified pathway
- Evan D. Rosen1,5,
- Chung-Hsin Hsu1,5,
- Xinzhong Wang2,6,
- Shuichi Sakai3,7,
- Mason W. Freeman2,
- Frank J. Gonzalez3, and
- Bruce M. Spiegelman1,4,8
- 1Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA; 2Lipid Unit, Massachusetts General Hospital, Boston, Massachusetts 02114, USA; 3Laboratory of Metabolism, National Cancer Institute, Bethesda, Maryland 20892, USA; 4Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
Abstract
PPARγ and C/EBPα are critical transcription factors in adipogenesis, but the precise role of these proteins has been difficult to ascertain because they positively regulate each other's expression. Questions remain about whether these factors operate independently in separate, parallel pathways of differentiation, or whether a single pathway exists. PPARγ can promote adipogenesis in C/EBPα-deficient cells, but the converse has not been tested. We have created an immortalized line of fibroblasts lacking PPARγ, which we use to show that C/EBPα has no ability to promote adipogenesis in the absence of PPARγ. These results indicate that C/EBPα and PPARγ participate in a single pathway of fat cell development with PPARγ being the proximal effector of adipogenesis.
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Footnotes
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Present addresses: 5Division of Endocrinology, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215, USA; 6Millennium Pharmaceuticals, 640 Memorial Drive, Cambridge, MA 02139, USA; 7Fuji Gotemba Research Laboratories, Chugai Pharmaceutical Company, Shizuoka 412-8513, Japan.
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↵8 Corresponding author.
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E-MAIL bruce_spiegelman{at}dfci.harvard.edu; FAX (617) 632-4655.
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Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.948702.
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- Received September 27, 2001.
- Accepted November 9, 2001.
- Cold Spring Harbor Laboratory Press
