During the acute phase (AP) reaction the expression of a series of liver-specific genes coding for secretory proteins is either stimulated or suppressed by different cytokines released by activated monocytes. Transforming growth factor beta (TGF-beta) is a cytokine that, first identified for its ability to regulate cellular growth, has been gradually recognized to modulate several other functions. We have investigated the effect of TGF-beta on the expression of acute phase genes in liver cells. We found that TGF-beta selectively induces a specific decreases in the amount of mRNAs of genes negatively regulated during AP reaction, like albumin and apolipoprotein A-I (ApoA-I). The inhibitory effect of TGF-beta on the expression of negative AP genes is primarily post-transcriptional and it is very likely to be mediated via an enhancement of the turnover of both albumin and ApoA-I mRNAs.
Morrone, G., Cortese, R., Sorrentino, V. (1989). Post-transcriptional control of negative acute phase genes by transforming growth factor beta. EMBO JOURNAL, 8(12), 3767-3771 [10.1002/j.1460-2075.1989.tb08553.x].
Post-transcriptional control of negative acute phase genes by transforming growth factor beta
Sorrentino, V.
1989-01-01
Abstract
During the acute phase (AP) reaction the expression of a series of liver-specific genes coding for secretory proteins is either stimulated or suppressed by different cytokines released by activated monocytes. Transforming growth factor beta (TGF-beta) is a cytokine that, first identified for its ability to regulate cellular growth, has been gradually recognized to modulate several other functions. We have investigated the effect of TGF-beta on the expression of acute phase genes in liver cells. We found that TGF-beta selectively induces a specific decreases in the amount of mRNAs of genes negatively regulated during AP reaction, like albumin and apolipoprotein A-I (ApoA-I). The inhibitory effect of TGF-beta on the expression of negative AP genes is primarily post-transcriptional and it is very likely to be mediated via an enhancement of the turnover of both albumin and ApoA-I mRNAs.File | Dimensione | Formato | |
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https://hdl.handle.net/11365/20960
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