Document Detail


The effects of colony-stimulating factor-1 on the distribution of mononuclear phagocytes in the developing osteopetrotic mouse.
MedLine Citation:
PMID:  9573014     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Colony-stimulating factor-1 (CSF-1), the primary regulator of mononuclear phagocyte (Mphi) production, exists as either a circulating or cell surface, membrane-spanning molecule. To establish transplacental transfer of maternal CSF-1, gestational day-17 mothers were injected intravenously with 125I-mouse CSF-1 or human rCSF-1, and the 125I-cpm or human CSF-1 concentrations were measured in fetal tissue, placenta, and fetal/maternal sera. Biologically active CSF-1 crossed the placenta and peaked in fetal tissue, placenta, and serum 10 minutes after injection. The role of CSF-1 in perinatal Mphi development was examined by studying the CSF-1-deficient osteopetrotic (csfmop/csfmop) mouse. Fetal/neonatal mice, derived from matings of either +/csfmop females with csfmop/csfmop males or the reciprocal pairings, were genotyped and tissue Mphi identified and quantified. In the presence of circulating maternal CSF-1 (+/csfmop mother), Mphi development in csfmop/csfmop liver was essentially complete at birth relative to +/csfmop littermates, but significantly reduced in spleen, kidney, and lung. In the absence of circulating maternal CSF-1 (csfmop/csfmop mother), Mphi numbers at birth were reduced in csfmop/csfmop liver relative to the offspring of +/csfmop mothers, but were similar in spleen, kidney, and lung. We conclude that CSF-1 is required for the perinatal development of most Mphi in these tissues. Compensation for total absence of local CSF-1 production by circulating, maternal CSF-1 is tissue-specific and most prominent in liver, the first fetal organ perfused by placental blood. However, because some Mphi developed in the complete absence of CSF-1, other factors must also be involved in the regulation of macrophage development.
Authors:
P Roth; M G Dominguez; E R Stanley
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Blood     Volume:  91     ISSN:  0006-4971     ISO Abbreviation:  Blood     Publication Date:  1998 May 
Date Detail:
Created Date:  1998-06-12     Completed Date:  1998-06-12     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  7603509     Medline TA:  Blood     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  3773-83     Citation Subset:  AIM; IM    
Affiliation:
Division of Neonatology, Department of Pediatrics, Albert Einstein College of Medicine, Bronx, NY, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Female
Fetal Blood / chemistry
Fetal Diseases / blood,  pathology
Heterozygote
Homozygote
Humans
Kidney / pathology
Liver / pathology
Lung / pathology
Macrophage Colony-Stimulating Factor / analysis,  deficiency,  genetics,  pharmacokinetics,  pharmacology*
Male
Maternal-Fetal Exchange
Mice
Mice, Inbred C3H
Mice, Inbred C57BL
Organ Specificity
Osteoclasts / pathology
Osteopetrosis / blood,  embryology,  pathology*
Phagocytes / drug effects*
Placenta / metabolism
Pregnancy / blood
Recombinant Proteins / analysis,  pharmacokinetics,  pharmacology
Spleen / pathology
Grant Support
ID/Acronym/Agency:
CA32551/CA/NCI NIH HHS; P30-CA13330/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Recombinant Proteins; 81627-83-0/Macrophage Colony-Stimulating Factor

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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