Regulation of neuronal cholecystokinin gene transcription

Hansen, Finn C. Nielsen Thomas V. O.

doi:10.1080/003655101753352068

Scandinavian Journal of Clinical and Laboratory Investigation

2001

DOI: 10.1080/003655101753352068

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Regulation of neuronal cholecystokinin gene transcription

Finn C. Nielsen Thomas V. O. Hansen

Abstract: Servais G. Diagnostic specificities and sensitivities of anti dsDNA, anti membrane DNA and anti nucleosomes autoantibodies. Scand J Clin Lab Invest 2001;61(Suppl 235):61-67.The aim of this study is to evaluate, from 369 routine sera of SLE and control patients, the worth of anti double stranded nuclear DNA, anti nucleosomes autoantibodies and anti membrane DNA for the diagnosis of SLE. Cell membrane associated DNA (mDNA) has been described on B lymphocytes and monocytes, but not on T cells. Antibodies to mDNA … Show more

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Cited by 7 publications

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ΔFosB indirectly regulates Cck promoter activity

et al. 2010

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Some of the important biochemical, structural, and behavioral changes induced by chronic exposure to drugs of abuse appear to be mediated by the highly stable transcription factor ΔFosB. Previous work has shown that ΔFosB overexpression in mice for 2 weeks leads to an increase in the expression of numerous genes in striatum, most of which are later downregulated following 8 weeks of ΔFosB expression. Interestingly, a large number of these genes were also upregulated in mice overexpressing the transcription factor CREB. It was unclear from this study, however, whether short-term ΔFosB regulates these genes via CREB. Here we find that 2 weeks of ΔFosB overexpression increases CREB expression in striatum, an effect that dissipates by 8 weeks. The early induction is associated with increased CREB binding to certain target gene promoters in this brain region. Surprisingly, one gene that was a suspected CREB target based on previous reports, cholecystokinin (Cck), was not controlled by CREB in striatum. To further investigate the regulation of Cck following ΔFosB overexpression, we confirmed that short-term ΔFosB overexpression increases both Cck promoter activity and gene expression. It also increases binding activity at a putative CREB binding site (CRE) in the Cck promoter. However, while the CRE site is necessary for normal basal expression of Cck, it is not required for ΔFosB induction of Cck. Taken together, these results suggest that while short-term ΔFosB induction increases CREB expression and activity at certain gene promoters, this is not the only mechanism by which genes are upregulated under these conditions.

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ΔFosB indirectly regulates Cck promoter activity

et al. 2010

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Interaction between cholecystokinin and the fibroblast growth factor system in the ventral tegmental area of selectively bred high- and low-responder rats

et al. 2013

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Individual differences in the locomotor response to novelty have been linked to basal differences in dopaminergic neurotransmission. Mesolimbic dopaminergic outputs are regulated by cholecystokinin (CCK), a neuropeptide implicated in anxiety. In turn, CCK expression is regulated by fibroblast growth factor-2 (FGF2), which has recently been identified as an endogenous regulator of anxiety. FGF2 binds to the high-affinity fibroblast growth factor receptor-1 (FGF-R1) to regulate the development and maintenance of dopamine neurons in the ventral tegmental area (VTA). However, the relationship between the FGF and CCK systems in the VTA is not well understood. Therefore, we utilized the selectively-bred low-responder (bLR; high-anxiety) and high-responder (bHR; low-anxiety) rats to examine the effects of repeated (21-day) FGF2 treatment on CCK and FGF-R1 mRNA in the rostral VTA (VTAr). In vehicle-treated controls, both CCK and FGF-R1 mRNA levels were increased in the VTAr of bLR rats relative to bHR rats. Following FGF2 treatment, however, bHR-bLR differences in CCK and FGF-R1 mRNA expression were eliminated, due to decreased CCK mRNA levels in the VTAr of bLR rats and increased FGF-R1 expression in bHR rats. Differences after FGF2 treatment may denote distinct interactions between the CCK and FGF systems in the VTAr of bHR vs. bLR rats. Indeed, significant correlations between CCK and FGF-R1 mRNA expression were found in bHR, but not bLR rats. Colocalization studies suggest that CCK and FGF-R1 are coexpressed in some VTAr neurons. Taken together, our findings suggest that the FGF system is poised to modulate both CCK and FGF-R1 expression in the VTAr, which may be associated with individual differences in mesolimbic pathways associated with anxietylike behavior.

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Enteroendocrine cell expression of a cholecystokinin gene construct in transgenic mice and cultured cells

Lay¹,

Bane²,

Brunkan³

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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CCK is predominantly expressed in subsets of endocrine cells in the intestine and neurons in the brain. We evaluated the expression of a CCK gene construct in transgenic mice and cultured cells to identify a genomic region that directs correct tissue- and cell-specific expression in enteroendocrine cells. The CCKL1 transgene contained 6.4 kb of mouse Cck fused to lacZ. Expression was evaluated in three transgenic lines (J11, J12, J14) by measurement of beta-galactosidase in tissue homogenates and frozen sections. Correct tissue-specific expression was observed, with beta-galactosidase activity detected in intestine and brain. However, there were differences seen in cell-specific expression in the intestine. Line J14 exhibited expression in CCK-endocrine cells, with expressing cells arising at the normal time during fetal development. However, transgene expression in line J12 intestine was limited to neurons of the enteric nervous system, which reflect an early fetal expression pattern for CCK. Analysis of an additional 15 transgenic founder mice demonstrated intestinal expression in 40% of transgenics, with expressing mice following either an endocrine cell pattern or a neuronal pattern in approximately equal numbers. CCKL1 transfection analysis in cultured cells also demonstrated enteroendocrine cell expression, with 100-fold enhanced activity in the enteroendocrine cell line STC-1 compared with nonendocrine cell lines. The results suggest that the minimal cis-regulatory DNA elements necessary for appropriate CCK expression in enteroendocrine cells reside within the 6.4-kb mouse genomic fragment.

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Regulation of neuronal cholecystokinin gene transcription

Cited by 7 publications

References 52 publications

ΔFosB indirectly regulates Cck promoter activity

ΔFosB indirectly regulates Cck promoter activity

Interaction between cholecystokinin and the fibroblast growth factor system in the ventral tegmental area of selectively bred high- and low-responder rats

Enteroendocrine cell expression of a cholecystokinin gene construct in transgenic mice and cultured cells

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