Apparent role of the macrophage growth factor, CSF-1, in placental development

Pollard, Jeffery W.; Bartocci, A.; Arceci, Robert J.; Orlofsky, Amos; Ladner, Martha; Stanley, E. Richard

doi:10.1038/330484a0

Cited by 471 publications

(212 citation statements)

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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%

“…CSF-1, the primary growth factor for macrophages, is synthesized to very high concentrations at the maternal-fetal interface by the uterine epithelium (15,16). Apart from the macrophages present in the undecidualized stroma, trophoblast express the CSF-1R suggesting that these are also target cells.…”

mentioning

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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“…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.…”

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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

132

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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“…In vivo animal studies, using ['25I]CSF-l as tracer, showed the half-life of CSF-I in the circulation to be approximately 10 min . During pregnancy the very high uterine synthesis of CSF-1 may contribute to the slightly elevated circulating CSF-I concentration (Bartocci et al, 1986;Pollard et al, 1987). Modest elevations in the circulating CSF-1 concentration are evident in disease states such as myeloproliferative disorders (Gilbert et al, 1989;Janowska-Wieczorek et al, 1991) and in ovarian cancer patients, in whom they were highly correlated with the presence of active disease (Kacinski et al, 1989a Cox (1972).…”

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confidence: 99%

Circulating levels of colony-stimulating factor 1 as a prognostic indicator in 82 patients with epithelial ovarian cancer

Scholl

Bascou²,

Mosseri³

et al. 1994

Br J Cancer

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Summary Serum samples from 82 patients with epithelial ovarian cancer, previously assayed for CA125, were assayed for circulating colony-stimulating factor 1 (CSF-1). An elevated CSF-1 concentration (>450 U ml-' or >5.42 ng ml-') was significantly associated with a worse survival (P = 0.02). The predictive value of raised CSF-1 levels was retained whether the first available sample for all patients (n = 82) or the first sample at the start of chemotherapy (n = 41) was considered. Mean CSF-1 levels (n = 14) dropped significantly during six courses of platinum-based chemotherapy (P= 0.02). Although an elevated CA125 concentration appeared to be a prognostic indicator in the total population (n = 82), it was not related to prognosis in the group of patients from whom samples had been drawn at the start of chemotherapy. In a Cox proportional hazards model, CSF-1, but not CA125, was significantly associated with outcome following adjustment for stage, grade and degree of surgical clearance.

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Apparent role of the macrophage growth factor, CSF-1, in placental development

Cited by 471 publications

References 0 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

Circulating levels of colony-stimulating factor 1 as a prognostic indicator in 82 patients with epithelial ovarian cancer

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