INT289724
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Butaprost-mediated SAT1 gene expression is potentiated by G? | |||||||||||||||
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We investigated the integrative signaling mediating the role of prostanoids on SAT1 expression in FPEP2 cells. | |||||||||||||||
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For example SAT1 gene expression was enhanced from a 5.9 fold increase to a 7.5 fold increase, whereas cytochrome P450, family 26, subfamily A, polypeptide 1 (CYP26A1) gene expression was repressed from an 18.0 fold increase to a 12.3 fold increase. | |||||||||||||||
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No significant elevation of SAT1 gene expression was observed following PGF treatment alone. | |||||||||||||||
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q cross-talk via AC3, such that siRNA knockdown of the AC3 isoform completely inhibited the potentiation of Butaprost-stimulated SAT1 expression by PGF. | |||||||||||||||
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However, co-stimulation of FPEP2 cells with Butaprost and PGF enhanced the Butaprost-stimulated expression of SAT1 significantly at all time points (P < 0.001). | |||||||||||||||
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To determine whether the PGF-mediated potentiation of SAT1 expression is mediated by the FP receptor, the cells were treated with the FP receptor antagonist (AL8810) in the presence/absence of Butaprost and/or PGF for 6 h. | |||||||||||||||
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As shown in Fig. 4A, Butaprost treatment alone significantly increased expression of SAT1 at all time points compared to vehicle treatment (P < 0.001). | |||||||||||||||
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As shown in Fig. 4C, ablation of AC3 expression reduced SAT1 mRNA expression in FPEP2 cells treated with the combination of Butaprost and PGF to the level observed following stimulation with Butaprost alone (P < 0.001). | |||||||||||||||
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A transgenic increase of SAT1 expression in mice showed a variety of defects such as hair loss, female infertility, impaired lipid metabolism and predisposition to develop pancreatitis [36]. | |||||||||||||||
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As shown in Fig. 4B, antagonism of the FP receptor completely abolished the potentiation of SAT1 expression by PGF without altering Butaprost-stimulated expression of SAT1. | |||||||||||||||
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As shown in Fig. 4B, antagonism of the FP receptor completely abolished the potentiation of SAT1 expression by PGF without altering Butaprost-stimulated expression of SAT1. | |||||||||||||||
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q cross-talk in FPEP2 cells, we assessed if the same isoform is involved in PGF-mediated potentiation of SAT1 expression. | |||||||||||||||
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These data demonstrate that Butaprost-regulated expression of SAT1 is augmented by PGF-FP receptor coupling. | |||||||||||||||
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