Temporal expression and location of colony-stimulating factor 1 (CSF-1) and its receptor in the female reproductive tract are consistent with CSF-1-regulated placental development.

Arceci, Robert J.; Shanahan, Fergus; Stanley, E. Richard; Pollard, Jeffrey W.

doi:10.1073/pnas.86.22.8818

Cited by 242 publications

(128 citation statements)

References 28 publications

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“…CSF-1 concentrations reach very high levels in the placenta and the CSF-1R is expressed on trophoblastic cells (16,24). Therefore, we questioned whether IDO expression was regulated directly or indirectly by CSF-1 by comparing expression in mice heterozygous or homozygous for the CSF-1 null mutation, Csf1 op (13).…”

Section: Ifn-␥ But Not Csf-1 Nor Tnf-␣ Regulates Ido Expression In Thmentioning

confidence: 99%

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Indoleamine 2,3-Dioxygenase Is Regulated by IFN-γ in the Mouse Placenta DuringListeria monocytogenesInfection

Mackler¹,

Barber²,

Takikawa

et al. 2003

The Journal of Immunology

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The tryptophan-catabolizing enzyme indoleamine 2,3-dioxygenase (IDO) is expressed in macrophages that have been differentiated in the presence of CSF-1 and is important in the containment of intracellular pathogens. IDO also appears to play a role in suppression of T cell responses in a variety of contexts. In the placenta, its enzymatic activity is believed to establish a chemical barrier that protects the fetal allograft from T cell-mediated immune aggression. We have studied the regulation of IDO in the utero-placental unit of mice following infection with the Gram-positive, intracellular bacterium Listeria monocytogenes that has a predilection for replication in the decidua basalis. IDO mRNA and protein expression is enhanced in the utero-placental unit following infection with L. monocytogenes. However, in contrast to the human where IDO is expressed by the CSF-1R-positive syncytial trophoblast, IDO is not expressed in murine trophoblastic tissue but instead is found in stromal cells of the decidua basalis and metrial gland and following infection, in endothelial cells. Using mice carrying null mutations in cytokine/growth factor genes, we explored the regulation of IDO in the placenta. Consistent with the absence of CSF-1R expression in the IDO-expressing cells of mice, neither the basal levels of IDO nor its induction following infection is affected by the absence of CSF-1. However, although the basal level of IDO is normal, the enhanced expression during Listeriosis is completely abrogated in the absence of IFN-γ, a cytokine required for the resolution of this infection. These data suggest that IDO plays a role in resolving bacterial infection in the placenta while at the same time maintaining a barrier to T cells whose presence might result in fetal rejection.

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Section: Ifn-␥ But Not Csf-1 Nor Tnf-␣ Regulates Ido Expression In Thmentioning

confidence: 99%

“…Total RNA was separated by electrophoresis (20 g/lane) in a 1.0% formaldehyde-agarose gel and then transferred to a nylon transfer membrane (Schleicher & Schuell, Keene, NH) as described (24). The blots were probed with gel-purified [ 32 P]dCTP-labeled cDNA probes (Prime-It RmT; Stratagene, Cedar Creek, TX).…”

Section: Northern Blottingmentioning

confidence: 99%

Indoleamine 2,3-Dioxygenase Is Regulated by IFN-γ in the Mouse Placenta DuringListeria monocytogenesInfection

Mackler¹,

Barber²,

Takikawa

et al. 2003

The Journal of Immunology

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show abstract

“…31,32 Indeed, the pleiotrophic roles for CSF-1 in reproduction, development of multiple organ systems, and maternal-fetal interactions during pregnancy by macrophage-mediated processes have also been well defined. 2,33,34 To determine the physiological relevance of CSF-1 as a component of the mammalian growth regulatory axis, CSF-1 was administered to neonatal mice. We report that CSF-1 administration to newborn mice increased body weight and kidney weight and volume and was associated with increased numbers of macrophages.…”

mentioning

confidence: 99%

Colony-Stimulating Factor-1 Promotes Kidney Growth and Repair via Alteration of Macrophage Responses

Alikhan

Jones

Williams

et al. 2011

The American Journal of Pathology

130

134

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Colony-stimulating factor (CSF)-1 controls the survival, proliferation, and differentiation of macrophages, which are recognized as scavengers and agents of the innate and the acquired immune systems. Because of their plasticity, macrophages are endowed with many other essential roles during development and tissue homeostasis. We present evidence that CSF-1 plays an important trophic role in postnatal organ growth and kidney repair. Notably, the injection of CSF-1 postnatally enhanced kidney weight and volume and was associated with increased numbers of tissue macrophages. Moreover, CSF-1 promotes postnatal renal repair in mice after ischemia-reperfusion injury by recruiting and influencing macrophages toward a reparative state. CSF-1 treatment rapidly accelerated renal repair with tubular epithelial cell replacement, attenuation of interstitial fibrosis, and functional recovery. Analysis of macrophages from CSF-1-treated kidneys showed increased expression of insulin-like growth factor-1 and anti-inflammatory genes that are known CSF-1 targets. Taken together, these data suggest that CSF-1 is important in kidney growth and the promotion of endogenous repair and resolution of inflammatory injury.

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“…Female reproductive tissues are the major sites at which M-CSF is produced. During pregnancy, synthesis of M-CSF markedly increases at the epithelium of the oviducts and the endometrium of the uterus (Arceci et al, 1989). Normal ovarian epithelium expresses M-CSF (Lidor et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Modulation of c-fms proto-oncogene in an ovarian carcinoma cell line by a hammerhead ribozyme

Yokoyama

Morishita²,

Takahashi³

et al. 1997

Br J Cancer

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Summary Co-expression of macrophage colony-stimulating factor (M-CSF) and its receptor (c-fms) is often found in ovarian epithelial carcinoma, suggesting the existence of autocrine regulation of cell growth by M-CSF. To block this autocrine loop, we have developed hammerhead ribozymes against c-fms mRNA. As target sites of the ribozyme, we chose the GUC sequence in codon 18 and codon 27 of cfms mRNA. Two kinds of ribozymes were able to cleave an artificial c-fms RNA substrate in a cell-free system, although the ribozyme against codon 18 was much more efficient than that against codon 27. We next constructed an expression vector carrying a ribozyme sequence that targeted the GUC sequence in codon 18 of c-fms mRNA. It was introduced into TYK-nu cells that expressed M-CSF and its receptor. Its transfectant showed a reduced growth potential. The expression levels of c-fms protein and mRNA in the transfectant were clearly decreased with the expression of ribozyme RNA compared with that of an untransfected control or a transfectant with the vector without the ribozyme sequence. These results suggest that the ribozyme against GUC in codon 18 of c-fms mRNA is a promising tool for blocking the autocrine loop of M-CSF in ovarian epithelial carcinoma.

show abstract

Temporal expression and location of colony-stimulating factor 1 (CSF-1) and its receptor in the female reproductive tract are consistent with CSF-1-regulated placental development.

Cited by 242 publications

References 28 publications

Indoleamine 2,3-Dioxygenase Is Regulated by IFN-γ in the Mouse Placenta DuringListeria monocytogenesInfection

Indoleamine 2,3-Dioxygenase Is Regulated by IFN-γ in the Mouse Placenta DuringListeria monocytogenesInfection

Colony-Stimulating Factor-1 Promotes Kidney Growth and Repair via Alteration of Macrophage Responses

Modulation of c-fms proto-oncogene in an ovarian carcinoma cell line by a hammerhead ribozyme

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