Regulation of human tissue factor expression by mRNA turnover.

Ahern, S; Miyata, Takeo; Sadler, J. Evan

doi:10.1016/s0021-9258(18)53975-2

Cited by 54 publications

(8 citation statements)

References 44 publications

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“…The induction of TF in response to stimuli is mainly regulated at the transcriptional level; but some stimuli may also increase the stability of TF mRNA and/or protein (Crossman et al 1990;Brand et al 1991;Ahern et al 1993;Reddy et al 2004) . The regulation of TF by IAA was well studied in vascular smooth muscle cells by the group of Chitalia.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of tissue factor induction by the uremic toxin indole-3 acetic acid through aryl hydrocarbon receptor/nuclear factor-kappa B signaling pathway in human endothelial cells

et al. 2018

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Chronic kidney disease (CKD) is associated with high risk of thrombosis. Indole-3 acetic acid (IAA), an indolic uremic toxin, induces the expression of tissue factor (TF) in human umbilical vein endothelial cells (HUVEC) via the transcription factor aryl hydrocarbon receptor (AhR).This study aimed to understand the signaling pathways involved in AhR-mediated TF induction by IAA.We incubated human endothelial cells with IAA at 50µM, the maximal concentration found in patients with CKD. IAA induced TF expression in different types of human endothelial cells: umbilical vein (HUVEC), aortic (HAoEC), and cardiac-derived microvascular (HMVEC-C). Using AhR inhibition and chromatin immunoprecipitation experiments, we showed that TF induction by IAA in HUVEC was controlled by AhR, and that AhR did not bind to the TF promoter. The analysis of TF promoter activity using luciferase reporter plasmids showed that the NF-B site was essential in TF induction by IAA. In addition, TF induction by IAA was drastically decreased by an inhibitor of the NF-B pathway. IAA induced the nuclear translocation of NF-B p50 subunit, which was decreased by AhR and p38MAPK inhibition.Finally, in a cohort of 92 CKD patients on hemodialysis, circulating TF was independently related to serum IAA in multivariate analysis.In conclusion, TF up-regulation by IAA in human endothelial cells involves a non-genomic AhR/p38 MAPK/NF-B pathway. The understanding of signal transduction pathways related to AhR thrombotic/inflammatory pathway is of interest to find therapeutic targets to reduce TF expression and thrombotic risk in patients with CKD.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of tissue factor induction by the uremic toxin indole-3 acetic acid through aryl hydrocarbon receptor/nuclear factor-kappa B signaling pathway in human endothelial cells

et al. 2018

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“…TF production is regulated at the gene expression level. 41,42 Incubation of HUVECs with TNF-α induced TF mRNA expression and subsequent TF protein synthesis (Fig. 2A and B).…”

Section: Discussionmentioning

confidence: 92%

The garlic-derived organosulfur compound diallyl trisulphide suppresses tissue factor function

et al. 2022

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“…Clones containing the mutations were identified by using the 32p_ labeled mutagenesis primers as probes (60) and were sequenced to verify the presence of the mutation (53). The chimeric c-fos promoter/cx2-globin gene construct (pfos/ox2) was made by excising the cx2-globin promoter and 5' NTR from pSV2Aneocx2 as a 575-bp EcoRI-NcoI DNA fragment and replacing it with a 595-bp EcoRI-NarI fragment containing the c-fos promoter (p3SFosMpg [1]). Two complementary oligonucleotides (sequences available on request) were included in the ligation to reintroduce the ac2-globin 5' NTR.…”

Section: Methodsmentioning

confidence: 99%

Erythroid Cell-Specific Determinants of α-Globin mRNA Stability

Weiss

Liebhaber

1994

Molecular and Cellular Biology

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Although globin mRNAs are considered prototypes of highly stable messages, the mechanisms responsible for their longevity remain largely undefined. As an initial step in identifying potential cis-acting elements or structures which contribute to their stability, we analyzed the defect in expression of a naturally occurring alpha 2-globin mutant, alpha Constant Spring (CS). The CS mutation is a single-base change in the translation termination codon (UAA-->CAA) that allows the ribosome to read through into the 3' nontranslated region (NTR). The presence of CS mRNA in transcriptionally active erythroid precursors and its absence (relative to normal alpha-globin mRNA) in the more differentiated transcriptionally silent erythrocytes suggest that this mutation disrupts some feature of the alpha-globin mRNA required for its stability. Using a transient transfection system, we demonstrate that in murine erythroleukemia cells the CS mRNA is unstable compared with the normal alpha 2-globin mRNA. The analyses of several other naturally occurring and site-directed mutant alpha-globin genes in murine erythroleukemia cells indicate that entry of a translating ribosome into the 3' NTR targets the message for accelerated degradation in erythroid cells. In contrast, both the CS and alpha 2-globin mRNAs are stable in several nonerythroid cell lines. These results suggest that translational readthrough disrupts a determinant associated with the alpha 2-globin 3' NTR which is required for mRNA stability in erythroid cells.

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Regulation of human tissue factor expression by mRNA turnover.

Cited by 54 publications

References 44 publications

Mechanisms of tissue factor induction by the uremic toxin indole-3 acetic acid through aryl hydrocarbon receptor/nuclear factor-kappa B signaling pathway in human endothelial cells

Mechanisms of tissue factor induction by the uremic toxin indole-3 acetic acid through aryl hydrocarbon receptor/nuclear factor-kappa B signaling pathway in human endothelial cells

The garlic-derived organosulfur compound diallyl trisulphide suppresses tissue factor function

Erythroid Cell-Specific Determinants of α-Globin mRNA Stability

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