Transcriptional regulation of the expression of macrophage colony stimulating factor

Rubin, Janet; Fan, Dongjie; Wade, A. Ayanna; Murphy, Tamara C.; Gewant, H.; Nanes, Mark S.; Fan, Xian; Moerenhout, Martine; Hofstetter, Willy

doi:10.1016/s0303-7207(99)00212-9

Cited by 19 publications

(14 citation statements)

References 33 publications

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“…54,56 However, the minimal promoter length required for normal tissue-specific and developmental expression has not been established, and modulation of CSF-1 gene expression by parathyroid hormone (PTH), tumor necrosis factor-␣, Il-1␣, and 1,25 (OH) 2 D3 observed in vivo is not reproduced with the 774-bp promoter construct. 55 The present studies establish regulatory regions required for normal CSF-1 gene expression that can be further investigated by deletion/mutation.…”

Section: Discussionmentioning

confidence: 71%

“…Previous studies of the regulation of CSF-1 gene expression have utilized CSF-1 reporter constructs containing 774 bp of the mouse CSF-1 promoter transfected into fibroblasts, monocytes, osteoblast-like, and COS-7 cell lines. 54,55 Several putative trans-acting factors for cis-acting elements in this region of the promoter have been identified, 54 and it has been shown that expression in different cell types is mediated by common and by cell type-specific transcription factors. 54,56 However, the minimal promoter length required for normal tissue-specific and developmental expression has not been established, and modulation of CSF-1 gene expression by parathyroid hormone (PTH), tumor necrosis factor-␣, Il-1␣, and 1,25 (OH) 2 D3 observed in vivo is not reproduced with the 774-bp promoter construct.…”

Section: Discussionmentioning

confidence: 99%

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Rescue of the colony-stimulating factor 1 (CSF-1)–nullizygous mouse (Csf1op/Csf1op) phenotype with a CSF-1 transgene and identification of sites of local CSF-1 synthesis

Ryan

Dominguez

et al. 2001

Blood

201

206

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Section: Discussionmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 99%

Rescue of the colony-stimulating factor 1 (CSF-1)–nullizygous mouse (Csf1op/Csf1op) phenotype with a CSF-1 transgene and identification of sites of local CSF-1 synthesis

Ryan

Dominguez

et al. 2001

Blood

201

206

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“…1c) and 774-nucleotide sequence from the murine MCSF promoter (Fig. 1e) (20). Further reduction in luciferase activity was seen with the addition of 300 M SNP to cells transfected with the constructs.…”

Section: Nitric Oxide Donors Inhibit the Luciferase Expression Of Mulmentioning

confidence: 85%

Nitric Oxide Donors Inhibit Luciferase Expression in a Promoter-independent Fashion

Fan

Roy

Zhu

et al. 2003

Journal of Biological Chemistry

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Nitric oxide (NO) is an important molecule with diverse bio-messenger functions including regulation of gene expression. Transcriptional studies using sensitive luciferase reporter systems have suggested that NO inhibits the promoter activity of a variety of genes. Here we report that NO donors (sodium nitroprusside, 2,2-(hydroxynitrosohydrazono)bis-ethanimine, and (؎)-(E)-4-ethyl-2-[(Z)-hydroxyimino]-5-nitro-3-hexen-1-yl-nicotinamide) decrease luciferase activity in a promoterindependent fashion in both viral and eukaryotic promoters, with a reduction to nearly 50% in the presence of 100 M NO donor. Addition of an SV40 enhancer downstream of the luciferase coding region shifted NO donor inhibition to the right, with inhibition at ϳ300 M. In contrast, when studied in a chloramphenicol acetyltransferase reporter, two promoters indicating inhibition by NO were unaffected. The decrease in luciferase activity was not caused by NO suppression of the luciferase enzyme. Real-time PCR data showed that luciferase mRNA half-life decreased by nearly half in the presence of NO donor (from 75 to 45 min). The SV40 enhancer prolonged luciferase mRNA half-life and somewhat blunted the NO effect. Our data suggest that exogenous NO inhibits luciferase activity in a dose-dependent manner through decreasing luciferase mRNA stability. Thus, the use of luciferase reporter systems to study transcriptional regulation by NO should be attempted with caution. Nitric oxide (NO)1 is a pluripotent regulatory gas with diverse biological effects on numerous enzymes, receptors, structural proteins, and transcriptional factors (1). Studies aimed at understanding the mechanisms by which NO has these myriad actions have represented one of the most rapidly growing areas of research during the last decade. Many reports have shown that NO alters proteins by regulating gene transcription through alterations in promoter specific activity; i.e. NO has been reported to suppress both Egr-1 (2) and PKG-I␣ (3) through control of their respective promoters. A partial list of similarly inhibited gene expression through regulation of promoter activity includes cytokines (4), cytochrome P450 enzymes (5), growth factors (6) as well as secondary inhibition of gene expression stimulatory by factors such as 1␣,25(OH) 2 D 3 (7) and estradiol (8). On the other hand, the ability of nitric oxide to up-regulate promoter activity has been less well reported, although many proteins are increased after exposure to nitric oxide (9 -11). Thus, the ability of nitric oxide to inhibit promoters seems to be widespread.We also found that nitric oxide inhibited the expression of a protein we were interested in; when we turned to transcriptional assays, we also measured effects of the permeable molecule on promoter-driven firefly luciferase. However, while studying a series of promoter deletions, we found that the effect of nitric oxide seemed to be nonspecific. This led us to consider whether our findings might be explained by a more general effect of NO on the luciferase reporter...

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“…Another interesting report shows the involvement of hydrogen peroxide in transforming growth factor-␤-induced CSF-1 expression (51). Very little has been reported on the transcriptional regulation of CSF-1 gene except for the recent reports elucidating the involvement of NFB and the NF1/CTF family of transcription factors in CSF-1 expression (52)(53)(54).…”

Section: Discussionmentioning

confidence: 99%

Concerted Action of Smad and CREB-binding Protein Regulates Bone Morphogenetic Protein-2-stimulated Osteoblastic Colony-stimulating Factor-1 Expression

Ghosh‐Choudhury

Singha

Woodruff

et al. 2006

Journal of Biological Chemistry

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Transcriptional regulation of the expression of macrophage colony stimulating factor

Cited by 19 publications

References 33 publications

Rescue of the colony-stimulating factor 1 (CSF-1)–nullizygous mouse (Csf1op/Csf1op) phenotype with a CSF-1 transgene and identification of sites of local CSF-1 synthesis

Rescue of the colony-stimulating factor 1 (CSF-1)–nullizygous mouse (Csf1op/Csf1op) phenotype with a CSF-1 transgene and identification of sites of local CSF-1 synthesis

Nitric Oxide Donors Inhibit Luciferase Expression in a Promoter-independent Fashion

Concerted Action of Smad and CREB-binding Protein Regulates Bone Morphogenetic Protein-2-stimulated Osteoblastic Colony-stimulating Factor-1 Expression

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