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- Title
B002: Pparγ activator inhibits il-6-induced c/ebpδ expression in vascular smooth muscle cells.
- Authors
Yang, Z.-H.; Takata, Y.; Nakamura, M.; Mori, S.; Jiang, Y.-N.; Okura, T.; Kitami*, Y.; Hiwada*, K.
- Abstract
PDGF α-receptor gene activation induced by inflammatory cytokines such as IL-1β and IL-6 is negatively regulated by PPARγ activator, troglitazone (TRO) or 15Δ-PGJ2, in vascular smooth muscle cells (VSMCs). This inhibitory effect is mainly regulated by a specific nuclear factor, CCAAT/enhancer-binding protein (C/EBP)δ. However, underling molecular mechanisms of the C/EBPδ gene regulation by PPARγ activator are still unknown.To identify a key factor that mainly regulates the C/EBPδ transcription after treatment with PPARγ activator, IL-6-induced C/EBPδ expression were evaluated by Western or Northern blotting in the VSMCs pretreated with TRO or 15Δ-PGJ2. Protein or mRNA levels of C/EBPδ induced by treatment with IL-6 (5 ng/mL) were significantly reduced by the pretreatment with TRO (0.1-10 μM) or 15Δ-PGJ2 (0.1-5 μM) in a dose-dependent manner. Functional promoter analyses revealed that TRO or 15Δ-PGJ2 suppressed C/EBPδ gene promoter activity through the inhibition of DNA-protein complex formation, STAT3 and acute-phase response element (APRE). Furthermore, TRO or 15Δ-PGJ2 induced dephosphorylation of STAT3. These results indicate that IL-6-induced transcriptional activation of the C/EBPδ gene is negatively regulated by PPARγ activator through the dephosphorylation of STAT3.Am J Hypertens (2000) 13, 153A-153A; doi:S0895-7061(00)00644-0
- Publication
American Journal of Hypertension, 2000, Vol 13, p153A
- ISSN
0895-7061
- Publication type
Article
- DOI
10.1016/S0895-7061(00)00644-0