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• W2013096096 abstract "In addition to important roles in the regulation of cell growth and cell restitution, both pro- and anti-inflammatory effects have been ascribed to TGFβ in intestinal epithelial cells. However, the mechanisms involved in TGFβ-dependent anti-inflammatory activities remain to be determined. In the rat intestinal epithelial cell line IEC-6, TGFβ attenuated the glucocorticoid-dependent increases in mRNA levels of the acute phase protein gene haptoglobin, and of C/EBP isoforms β and δ. Supershift assays demonstrated a TGFβ-mediated decrease in the binding of C/EBP isoforms β and δ to the haptoA and haptoC C/EBP DNA-binding sites from the haptoglobin promoter. Mutations of both HaptoA and HaptoC sites abolished the glucocorticoid-dependent activation and the TGFβ-mediated attenuation of the haptoglobin promoter, as assessed by transient transfection assays. TGFβ induced p42/p44 MAP kinase activities. Treatment with the MEK 1/2 inhibitor PD 98059 abolished TGFβ attenuation. These results suggest that C/EBP isoforms are involved both in the glucocorticoid-dependent induction and in the TGFβ-mediated attenuation of haptoglobin expression. Furthermore, p42/p44 MAP kinases may function in a TGFβ-dependent signaling pathway leading to attenuation of haptoglobin expression." @default.
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• W2013096096 date "1999-06-01" @default.
• W2013096096 modified "2023-09-24" @default.
• W2013096096 title "Attenuation of Haptoglobin Gene Expression by TGFβ Requires the MAP Kinase Pathway" @default.
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• W2013096096 doi "https://doi.org/10.1006/bbrc.1999.0808" @default.
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