Abstract | OBJECTIVE: METHODS AND RESULTS: SMC isolated from transgenic mice harboring the dominate-negative P465L mutation in PPARgamma ( PPARgamma(L/+)) exhibited greater proliferation and migration then did wild-type cells. Upregulation of ETS-1, but not ERK activation, correlated with enhanced proliferative and migratory responses PPARgamma(L/+) SMCs. After arterial injury, PPARgamma(L/+) mice had a approximately 4.3-fold increase in the development of intimal hyperplasia. CONCLUSIONS: These findings are consistent with a normal role for PPARgamma in inhibiting SMC migration and proliferation in the context of restenosis or atherosclerosis.
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Authors | Dane Meredith, Manikandan Panchatcharam, Sumitra Miriyala, Yau-Sheng Tsai, Andrew J Morris, Nobuyo Maeda, George A Stouffer, Susan S Smyth |
Journal | Arteriosclerosis, thrombosis, and vascular biology
(Arterioscler Thromb Vasc Biol)
Vol. 29
Issue 4
Pg. 465-71
(Apr 2009)
ISSN: 1524-4636 [Electronic] United States |
PMID | 19179641
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
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Chemical References |
- PPAR gamma
- Proto-Oncogene Protein c-ets-1
- Extracellular Signal-Regulated MAP Kinases
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Topics |
- Animals
- Carotid Artery Injuries
(metabolism, pathology)
- Cell Movement
- Cell Proliferation
- Cells, Cultured
- Disease Models, Animal
- Extracellular Signal-Regulated MAP Kinases
(metabolism)
- Hyperplasia
- Mice
- Mice, Inbred C57BL
- Mice, Transgenic
- Muscle, Smooth, Vascular
(enzymology, metabolism, pathology)
- Mutation
- Myocytes, Smooth Muscle
(enzymology, metabolism, pathology)
- PPAR gamma
(genetics, metabolism)
- Phosphorylation
- Proto-Oncogene Protein c-ets-1
(metabolism)
- Time Factors
- Wound Healing
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